A M AVATA

Dr. Mahesh C Kundagol

• Amavata is a conditon explained in Laghu
thrayees, but not in Brihat Thrayees.
• First explained in Madhava Nidana, by
Madhavakara who lived between 600-
700AD, that is one century after Vagbhata
• Later books like Yoga Ratnakara, Bhaishajya
Ratnavali etc quoted the slokas of Madhava
Nidana to explain the disease Amavata
without much change.
Nidana
ETIOLOGY & PATHOPHYSIOLOGY
 Samprifp_ti of Ama
Vata

Ahara Viharana Manasika

Viruddha Divva Chi nt a,
Sinidiaya ahara s:va.pna Shoka. Bhaya,
Snigdha ischaillata, Krodha
aharaJ
Guru
Ahara Dushti b Tridosha.
Agni
Prakopa mand:y,a
An1.a vish.a
SamaVata
Trika: sandhi
+ Rasavaha srotas:
t JPravesha
t
Daurbalya
Sandhi
Prasar Sandhi s h o t a
sth.abd!ata
a Dhamani. ShuJa
+
Dushti by Tridosha
Vyakti - - -i Amavata
3
 Sign
s

• These defective metabolic products with the

influence of Vata produces symptoms in
neck, lower back and all over the body and
produces stiffness.
 Samanya
Laxyan

• Bodyache
• Poor appetite, feeling thirsty, lethargic
• Heavyness in the body
• Feverish feeling
• Non inflammatory and non suppurative nature
 Ati Prabriddha
Laxana

• Very difficult to tolerate when becomes severe. Can also be

considered as difficult to treat when aggravates
• Severe pain in hand, foot, head, ankle, neck, low back,
knee and hip joints
• Pain and swelling is seen in different parts of body
• Pain will be severe as if bitten by scorpion.
(burning sensation and pain as if hit by stick)
Upadrav
a
 Complications
• Anorexia and feeling •
of Vomitting
heaviness over the body • Giddiness
• Loss of interest/drive • Fainting
• Bad taste in the mouth • Pericardial discomfort
• Polyurea •
and burning Constipation
micturition • Stiffness
• Hardness in the abdomen • Gurgling intestinal sounds
• Colicky pain • Other complications
• Reversal of normal
sleeping habbit
• Thirst
Doshik involvement and
Sadhyasadhyatha

Dosha Involvement
Pitta-Daha and Raga
Vata- soola
Kafa- Stimitata,
Kandu and Tama
P
rognosis
Sadhya-Ekadoshas
Yappya-Two dosha
 Line of
Management
1. Apatarpan
1. Langhan-Upabasa
2. Langhan Pachan-with Dipan Pachana Medicines
3. Dosabasechan- with Virechan and Vasti
2. Swedan
1. Rukshya Sweda
2. Snigdha Sweda
3. Upanaha Sweda
3. Rasayan Chikitsa (Naimittik Rasayan)
4. Pathya Aahar Bihar
Samanya Chikitsa-
Bhai.Ra
Yogaratnakara suggests Sneha
vivarjana
Importance of Eranda in Amavata
Bhaisajya Ratnawoli
suggests to use
Saindhawadi and
Brihat Saindhawadi
tel for local snehan
 Pathy
a
Aahar
Vastuka saka Aristha
Sunthi Adhrak
Ajawayan Maricha
Saindhav Hingu
Lasun Jeerak
Sahijan Parwar
Karela Yava
Kodrum Takra
Kulathha Gomutra
Usnodak Eranda
Vihar taila
Rukshyan Swedan
Langhan Chakraman
Mridu Byayam Ushna Bastra
 Apathy
a

• Curd • Vega dharan

• Fish • Ratri jagaran
• Gaggary • Bathing with cold water
• Milk • Ati Byabaya
• Viruddha aahara
• Purvi vayu sewan
 Medicines mentioned in B.R.
Lepa •Himsradi lepam
•Satapushpadi lepam
Kwatha •Rasnadi dasmoolkam
•Rasna saptkam
•Rasna panchkam
•Satyadi kwatham
•Rasnadi kwatham
•Maharasnadi kwatham
•Rasonadi kwatham

Churna •Amrutadi churnam

•Satpushpadhya churnam
•Hindgwadya churnam
•Vaishvanar churnam
•Punarnavadi churnam
•Pushpadhya churnam
•Aabhadya churnam
•Alambhuadya churnam
•Apar Alambhuadya churnam
Modaka and Pinda (Big size tablets) •Ajmodadi modak
•Aamvatagajasimho modaka
•Rasona pinda
•Maha rasona pinda
Guggulu •Vatari gugglu
•Yograja gugglu
•Vrut yoga raja gugglu
•Vyadhi shardula gugglu
•Simhanada gugglu
•Apara Simhanada gugglu
•Shiva gugglu

Ghrita and Taila •Sunthi ghritam

•Shrungaveradya ghritam
•Kanjikashatapala ghritam
•Prasarni tailam
•Dwipanchmuladya tailam
•Vijaya bhairava tailam
•Maha vijaya bhairava tailam
•Vrut saindava tailam
•Maha saindava tailam
 Continued…

Rasa •Hinguleshwar rasa

Yoga •Amrut manjari rasa
•Aamavatari gutika
•Aamvatari rasa
•Vatagajendra simha rasa
•Aamavataeshar rasa
•Triphaladi lauham
•Vidangadi lauham
•Aamapramathni vatika
•Aamavatadri vajra rasa
•Panchanana rasa lauham
 Management of Amavata

1. Diagnosis of Amavata by History taking and Investigations

(RF, CRP, ESR)
2. Management-
– Langhan Pachan by Amapachan Medicines like
Bishatinduk wati, Agnitundi wati.
– Doshawasechan by Virechan with Eranda Tail taken
orally with warm milk
– Sewdan- Baluka sewdan,
– Rasayan Chikitsa-Vatahar Chikitsa,Aswogadha
Compound, Maharasnadi kada, Aamvatari ras
etc.
– Symptomatic treatment if necessary.
– Pathyapathya recommendations
 Rheumatoid
Arthritis

Introduction:
• Commonest inflammatory joint disease seen in
clinical practice affecting approx 1% of
population.
• Chronic multisystem disease of unknown
cause.
• Characterized by persistent inflammatory synovitis
leading to cartilage damage, bone erosions,
 Aetiolog
y
 It is an autoimmune multisystem disorder.
Genetic Predisposition- Succeptibility increases with the pre-
sence of genes HLA DR4 and HLA DR1 in Indians and HLA
DW15 in Japanese.
Female gender is a risk factor, F:M =3:1 but before age 45 it
is 6:1. Prevalance increases with age.
 Although Rheumatoid arthritis may present at any age, but
incidence is more common in the third to fifth decade
 Smoking ( Current or ex-smoking) increases risk.
 Succeptibilty increases post partum by breast feeding?
 Early Menarche increases the risk
Relative incidence of joint
involvement in RA

MCP and PIP joints of hands & MTP of feet 90% metacarpophalangeal
Knees, ankles & wrists- 80% proximal interphalangeal

Shoulders- 60%
Elbows- 50%
TM, Acromio - clavicular & SC joints- 30% temporomandibular

Don’t forget the cervical spine!! Instability at cervical spine

can lead to impingement of the spinal cord.

Thoracolumbar, sacroilliac, and distal interphalangeal joints

(DIP)of the hand are NOT involved.
I n f l a m m e d synovial tissue (synovitis)
" Villous hyperplasia
• Intimal cell proliferation
• inflammatory cell ii1 u fil tr a tl
o n
T cells B, cells . macrophages and
plas,m a cells
• Production of cytokin es ,an d
p roteases
" [ncreas:ed vascnlarity
PIP
Swelling
 Swan Neck Defprmity
l debrmil\i
1.1ulmnn'

L:r.mil b9Qd,
toa:ir 1
VQi ,-u

© ·w , _ .r] eu r1'text corn.Hochiber et a! eds)

• Severe hype,rext ens· l on
of t o.
t h e 1 nt
I

the t h um , b with fl
1

f-
e r ph,- a x on of the J. .
angea
metacar
o -ii popha:l an,gea
(MCP) joint can occur; t his
is
cal le·d a d u·e -1 bilil, ,Z
(zigzag)
t yip e, or 90 -ang,1l,e
d- eform:it y.
1

mpaired
• With sim u lt an eo us,
thumb
n.st a:bllity, p1nch i· s _gr eat
Ulnar Deviation, MCP Swelling,
Left Wrist Swelling
H
 Extra-Articular
features
 Constitutional symptoms ( most common)-fatigue, weight
loss, anorexia and low grade fever
 Rheumatoid nodules(30%)
 Hematological-
 normocytic normochromic anemia
 leucocytosis /leucopenia
 thrombocytosis
 Felty’s syndrome-
 Chronic nodular Rheumatoid Arthritis
 Splenomegaly
 Neutropenia
o Caplan’s Syndrome-
• Pneumoconiosis following silica exposure
• Rheumatoid Arthritis
Rheumatoid
Nodules
Respiratory- pleuritis , pleural effusion, pneumonitis ,
pleuro-pulmonary nodules, ILD

CVS-asymptomatic pericarditis , pericardial effusion,

cardiomyopathy , mitral regurgitation

Rheumatoid vasculitis- mononeuritis multiplex,

cutaneous
ulceration, digital gangrene, visceral infarction

CNS- peripheral neuropathy, cord-compression from

atlantoaxial/midcervical spine subluxation, entrapment
neuropathies

EYE- kerato cunjunctivitis sicca, episcleritis, scleritis

on -Articul manifi st · o

IVi I
 Diagnos
is
ACR Criteria (1987)
1. Morning Stiffness ≥1 hour

2.Arthritis of ≥ 3 joints observed by physician.

3.Arthritis of hand joints-PIP, MCP, wrist

4. Symmetric arthritis
5. Rheumatoid nodules
6. Positive Rheumatoid Factor
7.Radiographic Erosions or periarticular osteopenia in
hand or wrist joints .

Criteria 1-4 must be present for ≥6 wks

Must have ≥4 criteria to meet diagnosis of RA
 2010 ACR/EULAR Classification
Criteria
A score of ≥6/10 is needed for classification of a patient as having
definite RA
A. Joint involvement
SCORE
1 large joint 0
2−10 large joints 1
1−3 small joints (with or without involvement of large joints) 2
4−10 small joints (with or without involvement of large joint) 3
>10 joints (at least 1 small joint) 5

B. Serology (at least 1 test result is needed for classification)

Negative RF and negative ACPA 0
Low-positive RF or low-positive ACPA 2
High-positive RF or high-positive ACPA 3
C. Acute-phase
reactants
(atleast 1 test result is needed for classification)
Normal CRP and normal ESR 0
Abnormal CRP or abnormal ESR 1

D. Duration of symptoms
<6 weeks 0
≥6 weeks 1
 Laboratory
Investigations

1. CBC ( TC, DC, Hb )

2. Acute phase reactants ( ESR, CRP )

3. Rheumatoid Factor (RF).

4. Anti- CCP antibodies (most specific ).

 Rheumatoid
Factor/RF
• Antibodies that recognize Fc portion of IgG.

• Can be IgM , IgG , IgA

• 85% of patients with RA over the first 2 years become RF positive.

•A negative RF may be repeated 4-6 monthly for the first two year of
disease, since some patients may take 18-24 months to become
seropositive.
•It is non specific to Rheumatoid Arthritis and may be positive in
other diseases such as Hepatitis C and in healthy older persons.
•PROGNISTIC VALUE- Patients with high titres of RF, in general,
tend to have POOR PROGNOSIS and MORE EXTRA ARTICULAR
MANIFESTATIONS.
Serum Anti Cyclic Citrullinated
Peptide Antibody
• Sensitivity of Anti-CCPA is similar to RF but Specificity is
about 95% in the diagnosis of RA.
• A positive test for anti-CCP antibodies in the setting of an
early inflammatory arthritis is useful for distinguishing RA
from other forms of arthritis.
• There is some incremental value in testing for the presence of
both RF and anti-CCP, as some patients with RA are positive
for RF but negative for anti-CCP and vice versa.
• The presence of RF or anti-CCP antibodies also has
prognostic significance, with anti-CCP antibodies showing the
most value for predicting worse outcomes.
 Other
Investigations

• Elevated Acute Phase Reactants( ESR,

CRP )
• Thrombocytosis
• Leukocytosis
• ANA in 30-40%
• Inflammatory synovial fluid Analysis
• Hypoalbuminemia
oRadiographic Features
 Peri-articular osteopenia
Uniform symmetric joint space narrowing
Marginal subchondral erosions
 Joint Subluxations
Joint destruction
Collapse

Ultrasound detects early soft tissue lesions.

MRI has greatest sensitivity to detect synovitis and
marrow changes.
 Manageme
nt
Goals of Management
• Focused on relieving pain
• Preventing damage/disability
• Patient education about the disease
• Physical Therapy for stretching and range of
motion exercises
• Occupational Therapy for splints and adaptive
devices
• Treatment should be started early and should be
individualised .
• EARLY AGGRESSIVE TREATMENT
 Treatment
modalities

NSAIDs
Steroids
DMARDs(Disease-
modifying antirheumatic
drugs)
Biological therapies
Surgery
 NSAID
s
Non-Steroidal anti-inflammatory Drugs
(NSAIDs) for symptom control :

1) Reduce pain and swelling by

inhibiting COX

2) Do not alter course of the disease.

3) Chronic use should be minimised.

4) Most common side effect related to GI

tract.
 Corticosteriods in
RA
Corticosteroids , both systemic and intra-articular are
important adjuncts in management of RA.
Indications for systemic steroids are:-
 For treatment of rheumatoid flares.
 For extra-articular RA like rheumatoid vasculitis
and interstitial lung disease.
 As bridge therapy for 6-8 weeks before the
action of
DMARDs begin.
 Maintainence dose of 10mg or less of
predinisolone daily in patients with active RA.
 Sometimes in pregnancy when other DMARDs
cannot be used.
Disease Modifying Anti Rhuematic
Drugs (DMARDs)

• Drugs that actually alter the disease course .

• Should be used as soon as diagnosis is made.

• Appearance of benefit delayed for weeks to months.

• NSAIDS must be continued with them until

true remission is achieved .
• Induction of true remission is unusual .
 DMARDs

Commonly used Less commonly used

Methotrexate Chloroquine
Hydroxychloroquine Gold(parenteral &oral)
Sulphasalazine CyclosporineA
Leflunomide D-penicillamine/bucillamine
Minocycline/Doxycycline,
Levamisole
Azathioprine,cyclophosphamide,
chlorambucil
 Limitations of DMARDs
1) The onset of action takes several months.
2) The remission induced in many cases is partial.
3) There may be substantial toxicity which requires
careful monitoring.
4) DMARDs have a tendency to lose effectiveness with
time-(slip out).
 These drawbacks have made researchers look for
alternative treatment strategies for RA- The Biologic
Response Modifiers.
 Biologics in RA
Cytokines such as TNF-α ,IL-1,IL-10 etc. are key mediators
of immune function in RA and have been major targets
of therapeutic manipulations in RA.
Of the various cytokines,TNF-α has attaracted
maximum attention.
Various biologicals approved in RA are:-
1) Anti TNF agents : Infliximab Etanercept
Adalimumab
2) IL-1 receptor antagonist : Anakinra
3) IL-6 receptor antagonist : Tocilizumab
4) Anti CD20 antibody : Rituximab
5) T cell costimulatory inhibitor : Abatacept
 Surgical
Approaches
• Synovectomy is ordinarily not recommended,
primarily because relief is only transient.
• However, an exception is synovectomy of the wrist,
which is recommended if intense synovitis is
persistent despite medical treatment over 6 to 12
months.
• Total joint arthroplasties, particularly of the knee,
hip, wrist, and elbow, are highly successful.
• Other operations include release of nerve
entrapments (e.g, carpal tunnel syndrome),
arthroscopic procedures, and, occasionally, removal
of a symptomatic rheumatoid nodule.