ROLE OF

PHYSIOTHERAPY IN RA
BY:HARDINI PRAJAPATI
MPT STUDENT
CARDIORESPIRATORY

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Rheumatological disorders
 rheumatology, a subspeciality of internal
med and ped,is devoted to the diagnosis &
therapy of rheumatoid dz.
 The term originates from greek RHEUMA
meaning “that which flows as a river or
stream” and the suffix-ology, meaning
“the study of”

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 Rheumatologists, mainly deals with
problems involving jts and the allied
conditions of connective tissues.
 Rheumatism, is a nonspecific term used to
describe any painful disorder affecting the
locomotor system; including
jts,ms,connective tissues, soft tissues
around jts and bones.

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 Rheumatism is also used to describe rh
fever affecting heart valves. However , the
med profession use specific terms to
describe rh disorders such as
RA,RF,AS,SLE,GOUT and more………….
 rheumatic disorder, is a nonspecific form
of med problems affecting the
heart,bones,jts,kidney,skin and lungs.

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 Rh disorders are like a common cold and
there are more than 100 types of
disorders are there, for eg;OA, RA, RF, AS,
GOUT, STILL’S DZ, SLE, SCLERODERMA,
SPONDYLITIS, TENDINITIS, VASCULITIS,
SJOGREN’S SYN, BURSITIS, AN,
DUPUYTREN’S DZ, PSORIATRIC
ARTHRITIS, PSEUDO GOUT, REITER’S
SYND, INFECTIOUS DISORDERS
…………………. AND MANY MORE.
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RHEUMATOID ARTHRITIS
 The term was first used by GARROD in
1858 but was not accepted by ARA as the
official terminology untill 1941.
 definition:
1. it is a systemic connective tissue disorder
which affects predominantly the synovial
jts, hence the term ‘RHEUMATOID DZ’
[golwalla]
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2. RA is a chronic inflammatory systemic dz of
young and middle aged adults, characterized by
destructive and proliferative changes in synovial
memb, periarticular stru, sk ms and perineural
sheaths. Eventually , jts are destroyed,
ankylosed and deformed. [ SAMUEL L TUREK]
3. It is a non suppurative systemic infl dz of of
unknown cause characterized by a symmetrical
polyarthritis affecting peripheral jts and extra
articular stur. [TIDY]

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EPIDEMIOLOGY
 1.5 million ppl affected in UK where as 2.1 million
are affected in USA.
 F:M, 3:1. there is a general increase in
prevalence for both sexes with incresing age.
 Age of onset is as young as 16 yrs but is
generally in the 20-55 yrs grp.
 There is some differences in the prevalence of RA
in certain subpopulations ,which suggests a
possible role for genetic or environmental factor
in etiology of the dz. eg

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ETIOLOGY
 Etiology of RA is still unknown.
 Current researches into the causes of RA
is based on the complex, but as yet
incomplete, appreciation of the fun of
IMMUNE SYSTEM.
 IMMUNE THEORY: based on the fact that
indi with RA produces antibodies to their
own Igs, hence there is some reason to
believe that RA is an AUTOIMMUNE
DISORDER.

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 INFECTIOUS THEORY: evidence suggests that a
variety of agents may initiate arthritis through a
no of mech.
 THEORY OF RF: RF are found in sera of approx
70% of all pts with RA. RF are antibodies specific
to IgG. Current theory suggests that RF arise as
antibodies to altered autologous [ pt’s own] IgG.
 RA occurs in the -nce of RF in a no of indi. Indi
with RF or seropositive , have increased freq of
subcutaneous nodules, vasculitis and polyarticular
inv.

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 GENETIC THEORY: RA has been associated
with increased HLA-D and HLA-DR [ D
related] antigens suggesting that certain
genes determine whether a host is more
or less at risk for an immunological
response that leads to RA.
 A ‘rheumatoid epitope’ has been identified
thr DNA typing of HLA-DR4 as a particular
sequence of amino acids common among
pts with RA.
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PATHOGENESIS
 The most widely held theory of pathogenesis is
that an immunologic response takes place in the
synovial tissues.
 An unknown exogenous antigen encounters the
defender cell, the lymphocyte, which is
transformed into a larger plasma cell, which
manufactures antibodies.
 Antigen+antibody= complex.
 Scavenger phagocytic cells engulf this complex.

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 These phagocytes contain enzyme producing
sacs, lysosomes, that destroy the complex. Some
of the lysosomes escape from phagocytes and
their proteases attack the cartilage and
synovium.
 Destruction of tissues produces debris that calls
for more phagocutic activity to remove debris.
Consequantly more phagocytes pour outs more
enzymez which create more desyruction and
further infl and arthritic process becomes self-
perpetuating.

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 The inflamed synovium forms a PANNUS ,
a granulomatous mass that grows over
and destroys cartilage, tendons and lig.
 This mass consists of 3 types of synovial
cells; TYPE A are phagocytic, TYPE B
resembles fibroblasts and TYPE C are
undifferentiated cells.

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PATHOLOGY
 The disorder is primarily a synovitis. Early
hyperemia, edema occur, lining cells
proliferate until they are three or more
layers thick and underlying tissue is
infiltrated with lymphocytes and plasma
cells.
 Villous processes gradually develop and
project into the jt cavity and they may
become necrotic and etruded into the jt.

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 The typical microscopic lesion is an area of
fibrinoid necrosis surrounded by fibroblasts
conspicuously arranged radially to the surface of
necrosis. Beyond this is an enveloping layer of
fibrous tissue.
 The rh units and infiltration of round cells are
prominent not only in synovium but also in
periarticular str.
 Leucocytes frequently are aggregated into round
collection that may encircle the blood vessel. And
increase amt of clear or turbid fluid accumulate in
the jt.

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 The synovium at the periphery forms a
pannus that grows progressively and
extends over the articular surface,
absorbing and replacling the articular
cartilage with fibrous connective tissue.
 Vascular granulation tissue from the
marrow extends towards the art surface &
destroys the cartilage from within bone.
The art cortex becomes thin and deficient
so that fibrous pannus forms the main
covering of bone.
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 The granulation tissue extends towards
opp art surface, merging with pannus
there, bridging the jt with granulation
tissue.
 A fibrous ankylosis sesults. The fibrous
tissue may under go metaplasia into
bone.within the articulating bones, the no
of trabecule become less and thin. Fibrous
proliferation thickenes the capsule.

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 Chronic inflammation can weaken jt
capsule and supporting lig, altering jt stru
and fun. Tendon rupture and fraying
tendon sheaths may produce imbalanced
ms pull on these pathologically altred jts.
This results in musculoskeletal
deformities, seen in advanced RA.

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Pathological changes in muscle:
 Nodular polymyositis
 Increase in size and no of sarcolemmic
nuclei, loss of striation, swelling of ms
fibres and localized collection of
lymphocytes.
 Damaged ms is replaced by fibrous tissue,
so loss of elasticity and contractile power
will result in restriction of ROM.

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Subcutaneous nodules:
 They are composed of the typical basic
rheumatoid unit, consisting of a central
necrotic zone, a surrounding layer of large
mono nuclear cells radially arranged and a
outer zone of dense connective tissue with
marked round cell infilteration.
 Found in 20% pts and +nt over pressure
areas.

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Circulatory changes:
 Redused blood flow in arterioles results in
cold and cyanosed distal extremities.
 Lymphnodes exhibit follicular hyperplasia
and there will be increased RE activity.

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CLASSIFICATION CRITERIA
 OLDER CRITERIA:
 For most of the 20th century, criteria had
allowed four classification of RA:
classical, definite, probable and possible.
 ARA criteria for diagnosis of RA:
1. Morning stiffness
2. Pain on motion or tenderness in at least
one jt
3. Swelling of one jt due either to soft tissue
or effusion or both
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4. Swelling of at least one other jt with an
interval free of symptoms no longer than
3 mths.
5. Symmetrical jt swelling
6. Subcutaneous nodules
7. Typical radiographic changes which must
include demineralisation in periarticular
bone as an index of infl.
8. Positive RF in serum
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9. Synovial fluid showing poor mucin clot
formation when added to dilute acetic
acid.
10. Histopathology of synovium consistent
with RA .
11. Characteristic histopathology of rh
nodules.
. S/S must be +nt for at least 6 weeks to
satisfy criteria 1 to 5.

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 RA may be classified as:
CLASICAL: if 7 criterias +nt
 DEFINITE: if 5 criterias +nt
 PROBABLE: if 3 criterias +nt

POSSIBLE: any of the following +nt at least

for 3 weeks;
Morning stiffness, H/O jt pain/swelling,
subcutaneous nodules, eievated ESR/CRP

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 NEW CRITERIA:
 New criteria were tested & established in
1987 based on a combination of signs,
sym and lab findings that have persisted
for a specific period of time.
 A diagnosis of RA is now established upon
the presentation of four of 7 listed criteria,
must lasted for at least 6 weeks.

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 The 1987 revised criteria for classification
of RA:
1. MORNING STIFFNESS; in and around the
jt lasting at least 1 hr before maximal
improovement.
2. ARTHRITIS OF 3/MORE JTS; at least 3 jts
simultaneously have had soft tissue
swelling or fluid observed by physician.
The 14 possible areas are rt/lt PIP, MCP,
wrist, elbow,knee,ankle & MTP jts

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3. ARTHRITIS OF HAND JTS; at least one
area swollen in a wrist, MCP , PIP
4.SYMMETRICAL ARTHRITIS; simultaneous
involvement of the same jt areas on both
sides of body.
5. RH NODULES; subcutaneous nodules over
bony prominences or extensor surface or
in juxta articular regions, observed by a
physician.

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6. SERUM RF; demonstration of abnormal
am of serum RF by any method for which
the result has been +ve in <5% of normal
control sub.
7 RADIOGRAPHIC CHANGES; typical of RA
on hand and wrist radiographs, which
must include erosion or unequivocal bony
decalcification localized in/most marked
adjacent to the involved jts.

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TYPES OF PRESENTATION
 CLASSICAL: pain ,stiffness and swelling of
small jts of hands and wrists. Symptoms
fluctuate in severity from day to day.
 PALINDROMIC: intermittent episodes of
pain, swelling and redness, usually of a
single jt followed by rapid return to normal
after several days.
 SYSTEMIC: wt loss, pleurisy and
pericarditis but minimal jt involvement.

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 POLYMYELGIC: pain and stiffness in sh
and hips with subsequent synovitis.
 MONOARTHRITIC: single jt involvement,
usually the knee.
 ACUTE ONSET: sudden overnight onset
with stiffness and pain.
 WITH GENERALISED LYMPHODENOPATHY

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STAGES OF RA
 From the clinical veiwpoint RA can be
divided into 3 stages:
1 STAGE 1: Reversible soft tissue
proliferation.
2 STAGE 2: Controllable but irreversible
soft tissue destruction and early cartilage
erosions.
3 STAGE 3: Irreversible soft tissue and
bony changes.

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SIGNS AND SYMPTOMS
 SYSTEMIC MANIFESTATIONS:
 Morning stiffness lasting more than three
months
 Anorexia, weight loss and fatigue are +nt
during early stages

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 ARTICULAR FEATURES:
 RA is marked by a bil and symmetrical
pattern of jt involvement.
 Clinically pt +nt with immobility and
cardinal features of infl.
 Arthralgia
 O/E crepitation which is audible, palpable
 Weakness of ms, lig, tendons leads to
deformities
 Fibrous ankylosis

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 INDIVIDUAL JOINT INVOLVEMENT:
 CERVICAL SPINE:
 Atlanto axial and mid cervical region are
commonly affected, specially at c1-c2 level
 Subluxation is common
 As spine is involved: neck pain, root pain,
radicular pain and some time UMN
features and vascular symptoms

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 TEMPOROMANDIBULAR JT:
 Inability to open the mouth fully
 Approximation of upper and lower teeths
may be altered
 CRICOARYTENOID JT:
 Not commonly involved
 Hoarseness of voice and can lead to
stridor

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 SHOULDER AND SHOULDER GIRDLE:
 GH, SC AND AC jts are involved
 Degeneration, pain and loss of ROM
 Scapular thoracic immobility
 Capsule and lig weakness
 Sh jt eventually becomes unstable
 Bursitis and tendinitis may result

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 ELBOW:
 Inflammation, capsular and lig distension,
jt surface erosion may lead to instability
and irregular/ catching mts
 Flexion contracture is common
 Ulnar nerve entrapment at its groove

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 WRISTS:
 Pain
 Dorsal subluxation of distal end of ulna puts the
ext tendons of 3,4 and 5 fingers in danger
 Early synovitis between carpal bones and ulna
leads to flexion contracture which ultimately
diminishes the ind’s ability to execute power
grasp
 Chronic infl of proximal row of carpals can lead to
volar subluxation of wrist and hand on radius

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 Chronic infl leads to the loss of radial lig. Support
and destruction of ECU and the fibro cartilage on
the distal side of the ulna. The attachment of this
restraining structures allows the proximal carpals
to slide down the distal radius towards the ulna,
creating the radial deviation of the distal raw of
the carpals in the wrist relative to the 2 bones of
the forearm where normally there are 5 to 10
degree of ulnar deviation.
 Stenosing tenosynovitis of the first dorsal
compartment of the wrist (DQ) ,may also occur.

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 HAND: MCP JTS:
 Soft tissue swelling is common
 The volar subluxation and ulnar drift of MCP
mainly due to laxity of capsule and lig and pulley
supporting tendons at MCP which results in
BOWSTRING effect
 This results in volar pull on proximal phalanx. At
the same time as the pully loosens the flexer
tendons are able to slip sideways typically in
ulnar direction. And thus the deformity of ulnar
drift with volar subluxesion begins. The tendons
of ED also can slide ulnary and contribute
additional deformity.

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 Radial deviation of carpals will furthure enhance
MCP ulnar drift as the phalanges try to
componset for the loss of normal ulnar deviation
at the wrist. This is known as ZIG-ZAG effect.
 There are additional predesposing factors that
contributes to this deformity:
1 The heads of the metacarpals are normally
sloped so more ROM in ulnar deviation than
radial deviation.
2 In many normal activities the fingers are pushed
in ulnar direction by the external forces.
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 PROXIMAL IP JOINT:
 Swelling of proximal IP joints produces a fussiform or
SAUSAGE like appearance in fingers.
 There are two characteristic deformities seen at PIP Joints.
 SWAN-NECK DEFORMITY:PIP hyper extension and DIP
flexion.
 This arises in three distinct ways, depending on the site of
initial involvement
1 Initial synovitis of the MCP
2 Volar capsule of the PIP is stretched in the later bands of
FDP move dorsally.
3 Rupture of ED at its insertion on DIP.

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 BOUTONNIERE DEFORMITY:DIP extension with
PIP flexion.
 This results due to chronic synovitis around PIP
which lengthens the tendon of ED at middle
phalanx and lateral bands slide volary.
 Bouchard’s nodes are found at PIP.
 DIP JOINTS:
 Heberden’s nodes are common.
 Mallet finger deformity due to rupture of tendon
of ED.

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 THUMB:
 Primary cause of deformity is synovial swelling.
 The fibers of dorsal hood mechanism over MCP is
affected.
 The exact mechanism of thumb deformities
depends on the particular combination of affected
structures. Actual presentation depends on the
site of initial synovitis, direction of imbalance of
muscles and the integrity of the surrounding joint
structures.

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1 Type 1 deformity, consisting of MCP
flexion with IP hyper extension without
involvement of CMC joint.
2 Type 2 deformity is assigned when the
CMC is subluxed and the IP is held in
hyper extension.
3 Type 3 deformity, there is CMC
subluxation and NCP hyper extension.

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 MUTILANS DEFORMITY/ OPERA GLASS HAND:
 Grossly unstable thumbs and severely deformed
phalanges are indicative of this deformity.
 The transverse folds of skin of thumb and fingers
resembles a folded telescope.
 Radiographic study of the bones of hand reveal
severe bone resorption, erosion and shortening of
MCP, PIP, RADIO-CARPAL and RADIOULNAR jts.
 The negative impact of this deformity on hand
fun and ADL is significant.

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 HIP JOINT:
 Less commonly affected
 Severe infl destruction of the femoral head
and acetabulam may push acetabulam
into pelvic cavity , a condition known as
PROTRUSIO ACETABULI.

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 KNEE JOINT:
 Most frequently affected
 Chronic synovitis results in distension of jt
capsule, attenuation of lig and destruction
of jt surface.
 Flexion-valgus deformity
 WIND-SWEPT deformity
 Backer’s / popliteal cyst

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 ANKLE AND FEET:
 Chronic synovitis accentuates the natural
tendency of the talus to glide medially and
plantarward, resulting in pressure on the
calcaneus and leading to hindfoot pronation. The
spring ligaments is also stretched, flattening
medial longitudinal arch.
 Calcaneal spur develops.
 As synovitis weakens the transverse arch, the
metatarsals spread and a splayed
forefoot/splayfoot may developed.
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 Metatarsalgia
 Hallux Valgus and Bunion(A painful
Bursitis over the medial aspect of first MTP
joint)
 When volar subluxation of the MTP
combines with flexion of PIP and hyper
extension of DIP, this condition is referred
to as Hammer toes.

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 The MTPs may also exhibit volar subluxation of
metatarsal head with flexion of PIP and DIP
joints, known as COCK-UP or CLAW TOES.
 As the capsules and intertarsal ligaments are
weakened and stretched, the proximal phalanges
move dorsally on the metatarsal head.
 Similar to conditions observed in the hand, the
long toe extensors bowstring over the PIP joints
while the flexors are displaced into the intertarsal
spaces.

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