BASIC SCIENCE

Orthopedic Infections

Acute hematogenous osteomyelitis

Definition: Acute suppurative inflammation.

Pathology

Age

Almost invariably a disease of children

When adults are affected , their resistance is lowered by ( diseases , drugs )

Organism

Gram +ve Staph. aureus (90%) , Strept. pneumonae , Staph. epidermidis , GB hemolytic strept.
(most common in neonates)

Gram -ve Hemoph. Influeza , E. Coli

Pseudomonas In puncture wounds , IV drug abusers

Salmonella Sickle cell disease

Opportunistic In immunocompromised patients ( fungal Actinomysis )

pathogens

Site

Children >>> Metaphysis ( esp. around knee )

1. Supplied by end arteries

2. Liable to trauma
3. Actively growing end
4. Strain ( Muscle & ligamentous attachment )

Adults >>> Spine ( DLS )

Route of infection: septic focus

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Predisposing factors

DM
Obesity
Trauma
Malignancy
Malnutrition
IV drug abusers
Immunosupression
Smoking
Systemic infections

Pathological stages

1. Inflammation
Acute inflammatory reaction with vascular congestion
Rise in intra-osseous pressure causing intense pain
2. Suppuration
At 2-3 days pus forms within the bone & spread into :
Horizontal direction: subperiosteal abscess , draining sinus
Vertical direction: into medulla >> thrombosis of nutrient vessels.
In children physis is a barrier that prevents spread to epiphysis & joint (except
in intracapsular metaphysis e.g. shoulder elbow hip ankle)
Vertebral infection can spread through the end plate, disc and into the next
vertebral body
3. Necrosis
At 7 days, rising pressure, vascular stasis, infective thrombosis and periosteal
stripping compromise the blood supply to the bone resulting in bone death
resulting in a sequestrum ( smooth , shiny white piece of cortical bone with
no periosteum )
4. New bone formation
At 10-14 days this forms from the deep surface of the stripped periosteum ,
surrounding sequestrum , forming the involucrum
If infection persists, pus discharges through ( Cloaca ) >> chronic
osteomyelitis
5. Resolution
With release of the pressure and appropriate antibiotics healing can occur
There may be remodeling or permanent deformity
NB - in 10% of cases there is more than one site of infection.

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Clinical Features

Children (invariably)

H/O of septic focus

FAHM ( fever, anorexia , headache , malaise )
Pain
Localized redness , hotness , swelling , tenderness
Limp or not weight bearing

Infants

Failure to thrive, drowsiness, irritable

Metaphyseal tenderness

Adults see later

Lab. studies

CBC : Leucocytosis ( ++ PMNL )

ESR: may be normal within the first 48 hours but rises rapidly and may exceed
100mm/hr; Its gradual decline indicates effective treatment

CRP

Rise within 6 h
Starts to decline after 2-3 d of effective ttt
Normalizes within 1 w of successful ttt
Best indicator for ttt success

Blood cultures Positive in 50% of cases

ASOT raised in 50%

Serological tests ( ASOT , IFAT , IHAT , Tuberculin test )

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Radiographic studies

X-rays

Essentially normal in the first 10-14 days

+/- soft tissue swelling shaddow
After 10-14 days , patchy rarefaction & sclerosis

Bone scan

Technetium99m

Gallium67

Indium111

MRI

++ T2 & -- T1 signal intensity,

++ T1 signal after Gadolinium

Aspiration and biopsy

positive culture in 80% of cases

D.D.

Acute cellulitis
Acute septic arthritis
Acute rheumatic fever
Ewing's sarcoma

Peltola criteria 2 out of 4

Pus aspiration
+ve blood culture
+ve clinical picture
+ve xray

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Management

Conservative ttt

Supportive : Analgesia , fluids , nutrition

Splinting
Antibiotics

o Empirically till C & S

o 4-6 w of IV antibiotics
o Monitored by CRP
o Recommendations

Staph Nafcillin / Oxacillin

Strept Benzyl penicillin
Gram -ve 3rd generation cephalosporins
MRSA Vancomycin
Pseudomonas Ciprofloxacin / Meronam
Salmonella Ciprofloxacin

Operative ttt

Indications

Failure to respond to antibiotics ( clinically CRP )

Subperiosteal abscess
Pus on aspiration
Chronic infection

Technique

Pus evacuation
Debridement
Drilling ( evacuate intraoss. pus / -- intraoss. pressure >> --pain )
Skin closed over a drain
2nd look may be needed
IV antibiotics

Complications
Metastatic infection
Septic arthritis
Chronic osteomyelitis
Pathological #
Growth disturbance

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Chronic non specific osteomyelitis

Pathology

Route of infection

Hematogenous spread
Inadequately treated acute osteomyelitis
Direct spread
Postoperative infection
Open #

Classification (Cierny)

Type I Medullary Limited to endosteal bone

Type II Superficial Limited to periosteal cortical bone
Type III Localised Involving whole thickness of cortical bone

@ one side of circumference

Type IV Diffuse Whole thickness infection

Causes of chronicity of infection

Sequestrum
Sclerosis surrounding bony cavity ( Involucrum )
Sinus ( 2ry infection )
Dormant bacteria in fibrous tissue

Clinical picture

H/O of acute OM
Pain
Swelling
Sinus discharging pus
Thick tender bone

Investigations

Labs : +ve if acute flare

Cultures : obtained from discharge

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Xray

Sequestrum
Involucrum
Patchy rarefaction , sclerosis
Bone thickening

Bone scan

MRI

Sinogram

Sinus injection with radiopaque material

Followed by xray or CT

Aim

Confirm bony origin

Detect extent of bony involvement

Complications : ++ risk of spread of infection & reactivation

CT-guided biopsy for pathology / C&S

D.D.

Malignancy : e.g. Ewing's sarcoma

Paget's disease

Treatment

Conservative ttt
As acute OM
But;
Antibiotics
not used empirically
IV for 6 W , followed by oral antibiotics for 3 M

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Surgical ttt
1- Radical debridement
Aim is to remove all dead and infected tissue and bone
Samples for: pathology , C&S

Type I Medullary Cortical de-roofing and medullary debridement

Type II Superficial Shallow decortication back to bleeding bone
Type III Localised Saucerisation and guttering
Type IV Diffuse Segmental resection and stabilised with ex-fix

2- Closure of dead space

Local flaps
Free flap transfer
Simple grafting
Useful for bone deficiencies of less than 4cm
Labour intensive
Vascularised bone graft
Heals as a segmental fracture
Indicated when defect is > 6 cm
Iliac crest for defects > 8cm
Fibula 6-35cm can be bridged
Bypass graft
Involves the establishment of a cross union between the fibula and tibia
proximally and distally to the defect which has been debrided and bone grafted
Ilizarov technique ( Distraction osteogenesis )
Acute shortening of the area debrided and the stabilised with ring fixator
Coticotomies then performed either above or below and then distraction
performed to correct length

3- Amputation:

Toxic ill patients

Diffuse infection & difficult reconstruction
Malignant transformation

Complications

As acute osteomyelitis

But Acute exacerbation instead of chronicity

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Garrs Chronic Sclerosing Osteomyelitis

Diaphyseal ( tibia ) , jaw D.D. Adamantinoma

Anaerobic organisms
Diffuse sclerosis with encroachment on medulla
No ( necrosis , pus , sinus , sequestrum )
No satisfactory treatment and antibiotic therapy does not affect course
ttt: drilling + cortical window
Recurrent for years then gradually subsides

Chronic multifocal recurrent osteomyelitis (CRMO)

Multiple , eccentric , metaphyseal , lytic lesions

Esp ( medial clavicle , distal tibia & femur )
No response to antibiotics
Only symptomatic ttt

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Subacute osteomyelitis
Relative mildness is due to

1. Organism being less virulent

2. Patient being more resistant

Age Children , young adolescents

Organism Staph aureus

Site Distal femur , Proximal & distal tibia

Brodie's Abscess

Well defined cavity

Round/ oval
Metaphyseal
Containing seropurulent fluid
Lined by granulation tissue
Surrounded by sclerosis

Clinical picture mild

Pain
Localized tenderness
Swelling
Normal temperature

Classification ( radiographic)
I Lucency A : well defined
B : ill-defined
II Metaphyseal with cortical bone loss
III Diaphyseal lesion
IV Onion skinning
V Epiphyseal lesion
VI Lesion in spine

Treatment

Exclude malignancy ( biopsy )

Curettage & antibiotics

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Septic arthritis
An emergency requiring prompt diagnosis & management

Epidemiology

Mostly in children < 2 years

Hip is the most commonly affected joint

Risk factors

Prematurity
Umbilical cord infection
Neonatal ICU

Route of spread

1. Haematogenous
2. Spread from metaphyseal osteomyelitis where the
metaphysis is intra-articular
3. Spread from contiguous soft tissue infection
4. Direct inoculation

Causative organism

GB hemolytic strept: Neonates

Staph aureus: Children
H. Influenza

Pathology

1- Inflammation : exudation , PMNLs infiltration

2- Suppuration
3- Necrosis: of articular cartilage , due to

o ++ Pressure
o Thrombosis
o Toxins
o Metalloprotinaze enz.

4- Spread : if no ttt
5- Healing : Resolution deformity Ankylosis

Clinical picture see acute osteomyelitis

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Investigations

Labs : see osteomyelitis

xray : may show joint space widening , subluxation
U/S: effusion
Aspiration : U/S guided , for cytology , C&S
MRI
Kocher's criteria : 90% chance of septic arthritis if 3 out of 4

1. WBCs > 12000

2. Inability to bear weight
3. Fever > 38.5
4. ESR > 40

Differential diagnosis

Child
Irritable hip (transient synovitis) see later

Adult
Gout
Pseudogout
Acute RA
OA
Psoas abscess

Treatment

There is no role for nonsurgical ttt

Confirm diagnosis by aspiration

Surgical drainage
Hips should always be drained surgically
Best approach anterolateral
Arthroscopic washout acceptable in knee but open drainage may be required

Postoperative IV antibiotics for 4-6 w

Rehabilitation

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Complications

Despite alarming XR changes there is a favorable outcome in many children

OA
Growth arrest
Septic dislocation
AVN
Deformity : e.g. Coxa vara

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Avascular Necrosis (AVN)

Osteonecrosis
Ischemic death of bone
Avascular necrosis affects epiphysis & subchondral bone
Bone infracts affect metaphysis & diaphysis
AVN sites in descending order:-
Femoral Head
Medical Femoral condyle
Humeral Head
Talus
Lunate & prox. Scaphoid
Capitellum
Metatarsal Heads

AVN hip

Epidemiology
30: 50 years

Bilateral in 80%

Anatomy Blood supply of femoral head

A. Ascending cervical arteries:
1. Extra capsular arterial ring: at base of NOF, formed by:
Ascending branch of MCFA : posterior
Ascending branch of LCFA : anterior
2. Ascending cervical arteries: Retinacular arteries
Piercing distal part of capsule
4 Groups (Anterior posterior medial lateral)
3. Subsynovial intracapsular ring: at margins of head cartilage
4. Epiphyseal arteries: penetrating head, lateral epiph. is the
most important
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B. Intramedullary nutrient artery:

C. Artery of Ligamentum Teres (Foveal):
Minor role in adults.
From medial circumflex Post branch of Obturator aa
Gives medial epiph. artery

N.B: Truetas lateral epiphyseal artery = Artery of Brodetti

Most important epiphyseal artery supply posterosuperior part of
head (WB area)

Risk Factor
Idiopathic Irradiation
Corticosteroid Caisson disease
Trauma Transplantation of organs
Sickel cell disease SLE
Hemophilia Hematologic (leukemia lymphoma)
Alcoholic Gaucher disease

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Pathognesis:
] AVN trauma:
Due to injury of Femoral Head blood supply (MCF)
Marrow cells survive 6 h of ischemia
Osteocytes survive 12-48 h of ischemia
Risk
- Femoral Head # 75-100%
- Transcervical # 50%
- Basitroch # 25%
- Hip dislocation # 10% early reduction
- Intertroch # Rare

] AVN out trauma:

Hypercoagulable state
Intraosseous pressure >>> Intraosseous HTN >>> Compartment
syndrome of Bone

Theories:
1. Fat cell hypertrophy: Corticosteroids
2. Fat embolism theory: In subchondral arterioles
3. Acute infraction: Direct injury
4. Intramedullary Hge
5. Accumulative cell stress: On marrow cells / osteocytes
6. Vascular stasis

Pathological stages :
1. Infarction: intact cartilage
2. Sclerosis: New bone surrounding dead bone trabeculae
3. Subchondral collapse: Collapse of necrotic segment
Crescent sign: linear # close to articular surface
Egg shell sign: separation of necrotic segment
4. Joint arthritis: due to fragmentation of necrotic segment

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Classification:
] Ficat & Artet staging

Pain Exam X-ray MRI Bone ttt

scan
0 Asymptomatic -ve ?? -ve No
+ IR -ve +ve +ve Core decompression
++ LOM Osteopenia +ve +ve Core decompression /
/ Sclerosis Strut graft
+++ LOM Collapse/ +ve +ve Strut graft / THR
Crescent /
Egg shell
++++ LOM Head +ve +ve THR
flattening,
Arthritis

] Steinberg: stages 0-3 as Ficat

Flattening of Femoral Head
Joint space narrowing
OA (Acetabular involvement)

] Shimizu: Risk of collapse depends on >>>> Extent,& Location

Extent < diameter : diameter >
diameter
Location Medial 1/3 of WB 1/3 : 2/3 > 2/3
surface
Collapse Rare 30% 70%

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C/P
Type of patient
H/O of risk factor (e.g. corticosteroids)
Hip pain: - Groin
- Insidious onset
- stairs / inclines / impact
loading
- Later pain rest
- Later night pain

Clicking: snapping of loose fragments

Gait: antalgic / Trendlenberg
LOM
Deformity: Flexion deformity (Thomas sign)
+ve Trendlenberg sign
Obligate ER passive Flexion
LLD < 2 cm

Imaging
X- ray: AP, Frog lateral see Ficat staging

MRI: highest sensitivity & specificity

Double Line sign
Low signal T1
Low signal T2
Bone scan: uptake high sensitivity in precollapse stage

SPECT: single photon emission computed tomography

Other investigations

Hemodynamic tests: Bone marrow pressure

To detect the cause: e.g. coagulation profile

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D.D.
1. OA: (Destructive / Sclerotic): acetabular changes from the start
2. Transient osteopenia of Hip: Marrow edema syndrome

AVN Transient osteopenia

Age 30: 40 > 40
Sex = >
Predisposing Coagulopathy Pregnancy in
Laterality Bilateral 80% Unilateral
Onset Insidious Acute
X-ray Sclerosis Osteopenia
collapse
Bone scan uptake Uptake (diffuse)
(localized)
MRI - Focal - Diffuse
- Double line sign - BM edema
(T1 , T2) - (T1 , T2)
Prognosis Progressive Spontaneous resolution

ttt

A) Conservative up to stage
Protected WB
Weight reduction
Bisphosphonates : collapse (in precollapse)
ttt of the cause: Alcohol, steroids

B) Operative:
Factors affecting ttt
Age
Head collapse (crescent)
Irreversible etiology
Extent of head involvement

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Core decompression () Bone graft

In precollapse stages
Aim >>> Intraosseous pressure
Stimulates healing (angiogenesis)
Methods: 8-10 mm hole through area of necrosis
3.2 mm drill into lesion 2:3 times
Electrical stimulation (PEMF) : alone / after core decompression
Trapdoor procedures: in
In precollapse stages
Open trapdoor through femoral neck cortex to access area of
necrosis debridement + Bone graft.
Strut grafting: (Fibula Tibia Iliac crest)
Biomechanical support of necrotic segment
In precollapse stages
With core decompression
N.B. Vascularized Free Fibula transfer
In precollapse / collapse stages
Fibular strut graft under subchondral bone through large core
hole
Vascularized pedicle flaps:
a) Posterior: Quadratus Femoris
b) Anterior: Tensor Fascia lata
Rotational osteotomy:
In small lesions (< 50%) which can be rotated away from
WB area.
Through intertroch osteotomy
Making joint later more difficult
Hip Arthrodesis:
In young patient, advanced disease
Single unilateral joint affection
Arthroplasty:
THA: advanced collapse, arthritis
Hemiarthroplasty & resurfacing are rarely used
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AVN Knee
Introduction: 2 types
Spontaneous osteonecrosis of the Knee (SONK)
Secondary osteonecrosis of the Knee

Epidemiology:
- >
- 30-50 years (older in SONK)

Pathophysiology:
Etiology: Unknown
Vascular theory: vascular HTN
Trauma theory: Subchondral insuff.#
Caused by meniscal root tear

Risk Factors: see Hip

Site: MFC > LFC > Plateau

SONK: single compartment affection (MFC)
Secondary: more than one compartment + metaphysis

Pathology: See Hip

Prognosis: Self limiting

C/P:
Knee pain: see Hip
Effusion
LOM
Localized tenderness

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Imaging:
X- ray:
- Lesion is (( crescent shaped (SONK), wedge shaped (secondary) ))
- X- ray of Hips also required
- Staging: see Hip
Other investigations: see Hip

D.D.
1. OCD: in Lateral aspect of MFC, adolescents
2. Transient osteoporosis: - younger age
3. Bone bruises: #
4.
SONK Secondary osteonecrosis
Age >50 years 30-50 years
Lesion Crescent shaped Wedge shaped
No Single Multiple comp. +
compartment metaphysis

ttt:

A) Conservative: 1st line of ttt >>> Better results in SONK

- NSAIDs
- Protected WB
- Physiotherapy: Quadriceps strengthening

B) Operative: if failed conservative

Arthroscopic debridement: removal of small fragments
Core decompression: if extra-articular lesion
Mosaicoplasty: if large lesion in young patient
High tibial osteotomy: if angular malalignment
TKA: if large lesion collapse

N.B:- Uni-compartmental arthroplasty may be done if single lesion

(SONK)

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AVN Shoulder

Anatomy: Blood supply of Humeral Head

1. Posterior circumflex humeral artery: main blood supply
2. Ascending branch of anterior circumf. artery & arcuate artery

Pathophysiology: see Hip

Site of Lesion: superior middle portion of Head

Classification: Cruess classification

Infarction Changes on MRI out x- ray
Sclerosis Wedge, mottled sclerosis
Crescent Crescent sign = subchondral #
Collapse Flattening of Head

Arthritis Glenoid affection

C/P:
- Shoulder pain: insidious onset
- LOM
- Crepitus
- Weakness (RC Deltoid)

Imaging:
X-ray: staging as in Hip
MRI: see Hip
ttt:
A) Conservative 1st line of ttt
* Analgesics
* Physiotherapy
* Restrict overhead activity
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B) Operative:
1. Core decompression: Early, stage ,
2. Humeral Head resurfacing: stage , focal defect, good bone
stock
3. Hemiarthroplasty: stage ,
4. Total shoulder arthroplasty: stage

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Osteoarthritis

Introduction
Non inflammatory degenerative joint disease
Characterized by progressive loss of articular cartridge
Associated new bone formation & capsular fibrosis.

Epidemiology
Commonest joint disease
> 60 years

Knee > Hip > Hand > Spine, Other joints

Pathophysiology
Etiology:
Primary Secondary
Age > 60 years Age from 20 to 30 years
Unknown 1. Congenital: e.g. DDH, Perthes,
Multifunctional dysplasia
Due to disparity between: 2. Traumatic: intra artic. #,
Wear: stress ligament injury
Repair: chondrocyte 3. Infection: Septic / TB arthritis
response 4. Metabolic: ochronosis
Either; hemochromatosis
load on normal joint 5. Endocrine: Acromegaly
Normal load on abnormal joint Hyperparathyroidism
6. Neuropathies: DM, charcots
7. Hemorrhagic: hemophilia
8. Others: Obesity , Ehler-Danlos
syndrome

Pathogenesis (Theories):
1. Fatigue of collagen meskwork: loss of proteoglycans
2. Subchondral micro #: Repetitive loading
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Pathology:
1. Gross changes:-
* Articular cartilage >>>> Softening, Fibrillation, Erosion.
* Areas of ulceration exposure of subchondral bone.
* Osteophytes development
Vascularization of Subchondal bone
Capsule Traction
Synovial Metaplasia
Cartilage Proliferation
Endochondral Ossification

2. Microscopic changes:
Early Late
Superficial splits Extensive Clefts
Chondrocyte clusters Cysts amorphous material

Subchondral osteoblastic activity Bone necrosis

3. Molecular changes: ( vs Aging >>> see Articular cartilage )

Water content Proteoglycan quantity & size
IL -1 Quantity of collagen
Chondrocyte activity & proliferation Cross-linking of collagen

Metalloptnaze Modulus of elasticity

Cathepsin B,D

N.B. Genes Linked to OA:-

Vit D Receptors
Estrogen Receptors
Inflammatory Cytokines (IL-1 , IL-4 , Matrilin-3 , BMP-2 , BMP-5)

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C/P
Type of patient: old age, +ve family H/O
Joint pain: gradual onset
Intermittent course
in the morning
Swelling (Effusion)
Stiffness: ROM
Localized tenderness
Deformity Hip: Flex, ER, Adduction
Knee: Flexion, varus
Special characteristics:
Hip: +ve FABER test, Thomas test, Trendelenburg Test
Hand: Herberdens nodes at DIPJ (compared to Bouchard
nodes in RA)

Imaging
X-ray Fairbanks Changes
Joint space narrowing
Subchondrial sclerosis
Subchondrial cysts
Marginal osteophytes
Bone destruction & joint
deformity (late cases)

CT: preoperative planning

MRI: when AVN suspected

Bone scan: uptake (vascularity & new bone formation)

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ttt
A) Conservative 1st line of ttt
1. Medical ttt: NSAIDs, Glucosamine, Chondroitin.
2. Weight reduction: If BMI> 25
3. Activity modification: Avoid stairs, inclines, squatting
4. Physiotherapy
5. Bracing / Assist devices (Cane/ Crutch)
6. Intraarticular injection
Corticosteroid: Antiinflammatory
Hyaluronic Acid: Backbone of proteoglycan chain

B) Operative:
Indications
Progressive in pain
Activity
Stiffness
Marked Deformity
X-ray signs of joint destruction

1- Arthroscopic Debridement:
Mensical / Labral tears
Mechanical Symptoms; Locking, Clicking
Loose Bodies
Synovitis
Chondral Flap Tears

2- Corrective Osteotomy:
Redistribute WB Load
In young active patients
When disease affects predominantly one compartment
Unfavorable when arthroplasty is planned
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3- Arthrodesis:
Young patients severe arthritis, unilateral, single joint.

4- Arthroplasty > 60years, advanced OA

- Hip (Hemirathroplasty THA).
- Knee (TKA- Unicompartmental arthroplasty).
- Shoulder (Total shoulder arthroplasty hemiarthroplasty
reserved shoulder arthroplasty).

5- Other procedure:
Hip: Reaction arthroplasty: if
Incurable infection
Noncompliant patient recurrent THA dislocation
Non Ambulator
Failed Fusion
Knee: procedures for isolated Patellofemoral arthritis
lateral retinacular release
Patellofemoral replacement
Patellectomy

Complications
A Ankylosis
B Loose Bodies
C Bakers Cysts
D Deformities

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Rheumatoid Arthritis (RA)

Definition
Chronic, Systemic, Progressive, Autoimmune, Inflammatory disorder
affecting joints & other organs.

Epidemiology
Most common chronic inflammatory joint disorder
Age: 25: 50 years (40 years)
: 4:1
Hand Knee Hip CS

Etiology Unknown
1. Genetic susceptibility:
a) More common in 1st degree relative & twins.
b) Genetic marker: HLA-DR4

2. Immunological: Autoimmune process

a) Autoantibodies (RF): against patients IgG.
b) Associated other autoimmune diseases e.g. Hashimotos
thyroiditis.

3. Infections:
a) Viruses: EBV
b) Bacteria: Streptococci

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Pathology

I. Articular:- RA is a disease of SYNOVIUM

Stage 1: Synovitis
Vascular congestion Effusion
Villous formation (Synoviocytes proliferation).
Inflation by PMNs, Lymphocytes & plasma cells.
Stage 2: Destruction
Pannus of granulation tissue creeps over articular surface.
Erosion of cartilage & bone destruction.

Stage 3: Deformity
Articular destruction
Capsular stretching
Tendon rupture

II. Extra-Articular:-

Salivary & Lacrimal secretion >>> (Sjgren syndrome)

Lymphadenopathy & Splenomegaly (Felty's syndrome)
Pleurisy + Pulmonary nodules (Caplan's syndrome)
Vasculitis
Skin: S.C. nodules over pressure areas & extensor tendons
Renal amyloidosis
Myopathy

Prognosis
Significant advances in pharmacologic management have led to a
decrease in surgical intervention

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C/P
Type of patient: 40 years - - +ve family H/O
Joints affected: Bilateral, Symmetrical, Polyarticular
Common [Hand Knee Hip CS]
Rare [TMJ SCJ]
Never [DIPJ, Sacroiliac Joint]
Early:
Pain: insidious onset + limping.
Morning stiffness
Affected joint: swelling, tenderness, warmth, LOM, crepitus,
synovial hypertrophy.
Deformity (discuss)
Disability
Pathological #
Deformities:
Hip: Flexion deformity.
Knee: valgus + Flexion deformity.
Foot: Valgus heel , Hallux valgus & Loss of arch support
Spine: atlantoaxial subluxation
Hand: e.g.
Fusiform Finger (swollen PIPJ)
Radial deviation of the wrist
Ulnar deviation of MCPJ
Bouchards nodules
Boutonniere deformity
Swan neck deformity
Z deformity of thumb
Extra-Articular:
General : fever , constitutional manifestations
Skin: atrophy ulcers S.C. nodules
Eye: Sjogren's $ , scleritis
Heart: pericarditis , effusion , coronary vasculitis
Lung: pleurisy , effusion , pulmonary nodules
Kidney: Nephrotic $ , CRF
Muscle wasting
Hematological : anemia , splenomegaly, L.N. enlargement
Nerve compression syndrome

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Lab studies
Blood
Anemia
ESR, CRP
RF 80% nonspecific (TB- SLE- SBE)
ANA 30% nonspecific
ACCP ((anti cyclic cetrolinated peptide))
Synovial Fluid aspiration
RF +ve
ptn C, Glucose

Imaging
X-ray Larsen Dale radiographic index.

: Juxta-articular osteopenia, soft tissue swelling.

: Narrow joint space Bilateral, symmetrical.
: Erosion = Mouse-bite erosion
: Deformity

N.B.
No osteophytes.
Hand & CS x-rays are important.

Diagnostic criteria (ARA): American Rheumatoid Association

RA is diagnosed in the presence of 4 or more of the following criteria
1. Morning Stiffness: at least 1 hour
2. Arthritis 3 joints
3. Hand joints affection
4. Symmetrical affection
5. Rheumatoid nodules (over extensor)
6. +ve RF
7. Radiographic changes (Erosion Periarticular porosis )

110 Dr. Mahmoud Desouky

 BASIC SCIENCE

ttt
No cure for RA
Aim of ttt
Cosmoses , Function
Pain , Damage

A. General measures:
- Reassurance
- Rest: bed rest, splints
- Physiotherapy

B. Medical ttt:
1. NSAIDs: - Aspirin
- Indomethacin 50 mg t.d.s
2. Corticosteroids: prednisone 7.5 mg/day
3. Disease-modifying anti-rheumatic drugs (DMAR)
Affect natural course of the disease through immune mechanisms
e.g. Penicillamine Gold Sulphasalazine
4. Immunosuppressive Drugs: e.g. Methotrexate
5. Biologic agents:
TNF antagonists (Etanercept , Infliximab)
IL-1 antagonists (Anakinra)
Others (Rituximab)
6. Intraarticular corticosteroid injection

C. Surgery:
- Synovitis Synovectomy.
- Prevent deformity.. Tendon repair, joint stabilization.
- Deformity
Reconstructive (Arthroplasty)
Arthrodesis (not done bilateral).
Osteotomy: not done (as it doesnt remove cartilage which is
source of inflammation.

111 Dr. Mahmoud Desouky

 BASIC SCIENCE

N.B.
Principles of operative ttt:
Proximal joints >>> Distal
Tendons >>> Joints
Use of immunosuppressive drugs may lead to ++ risk of postoperative
infections
>>> should be discontinued 10-14 days before surgery till wound closure

Rheumatoid arthritis in different joints

Rheumatoid hip
Protrusio acetabulae

Rheumatoid knee
Synovectomy
TKA + resurfacing of patella

Rheumatoid shoulder
Associated with
1. RC tear
2. Central glenoid wear

Rheumatoid elbow (S.C. nodules)

Synovectomy + Radial head resection
Interposition arthroplasty: in young patients
Total elbow arthroplasty: in elderly

Rheumatoid foot
MTPJ hyperextension >>> MTPJ arthrodesis + Lesser MTPJ resection
Talonavicular arthritis >>> TN fusion
Subtalar arthritis >>> triple arthrodesis
Hallux valgus >>> Keller osteotomy , 1st MTPJ arthrodesis

112 Dr. Mahmoud Desouky