Ain Shams University The Hip - Orthopedic Dept., King Fahd

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Quick Guide Anatomy and Biomechanics Osteonecrosis Arthritis Miscellaneous conditions Arthroplasty Ain Shams University The Hip Mohamed Sobhy اﻟﺮﺣﻴﻢ اﻟﺮﺣﻤﻦ اﷲ ﺑﺴﻢ

Transcript of Ain Shams University The Hip - Orthopedic Dept., King Fahd

Quick Guide

♦ Anatomy and Biomechanics

♦ Osteonecrosis

♦ Arthritis

♦ Miscellaneous conditions

♦ Arthroplasty

Ain Shams University

The Hip Mohamed Sobhy

بسم االله الرحمن الرحيم

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Hip Anatomy & Biomechanics TTyyppee Ball and socket synovial joint OOss CCooxxaaee = the hip bone (Ilium + pubis + ischium)

KKrraauussee’’ss bboonnee: small bone (2ry ossific center) in the triradiate cartilage bet ilium, ischium, and pubis AAcceettaabbuulluumm

• Bony cavity faces obliquely: o Forward ........................................... 12º from sagittal plane o Outward .......................................... o Downward ..................................... 60º from axial plane (labrum make this angle 45-50º)

• A line through the circumference is at 40º opening posteriorly from the sagittal plane and at 60º from the coronal (horizontal) plane

FFeemmoorraall hheeaadd • Forms 2/3 of a sphere • Articular surface is thicker on the mediocentral part and thinnest on the periphery • The Joint reaction force usually acts on the superior quadrant

2 BBlloooodd ssuuppppllyy ooff ffeemmoorraall hheeaadd

1. Medial circumflex femoral a. .......................... most important supply, from profunda a. then run posteriorly bet. Pectineus and iliopsoas, above the lesser trochanter and posterior to the neck, to find the obturator externus tendon & run below it an deep to the quadratus femoris, where it gives some branches to the GT............................ mainly form the EEXXTTRRAA--CCAAPPSSUULLAARR AARRTT RRIINNGG that gives TTRRUUEETTAA’’SS LLAATTEERRAALL EEPPIIPPHHYYSSEEAALL AARRTTEERRIIEESS that pierce the supero-lateral capsule, beneath the synovial reflection, till it reaches the metaphysio-epiphyseal junction where it share in the formation of the subsynovial IINNTTRRAA--AARRTTIICCUULLAARR AARRTTEERRIIAALL RRIINNGG, that gives branches that enter the head just distal to the articular junction

2. Lateral circumflex artery ................................... supplies the inferior portion, from profunda femoris also and passes anterior to iliopsoas tendon till it reaches the Intertrochanteric line running over it supplying the capsule and muscles ................... and share the extra-capsular ring anteriorly, and gives the ascending cervical vv. at regular intervals, anteriorly these pierce the capsule at the inter-trochanteric line

3. Artery of the ligamentum teres ................... minor blood supply in adult (post br. of obtuator a.) only supplies the area just beneath the fovea centralis

FFeemmoorraall nneecckk

• The angle of anteversion ................................ ≈ 12º in adults • Neck shaft angle ................................................ ≈ 125º (90-135º) • >125º = coxa valga. < 125 º = coxa vara

CCaallccaarr FFeemmoorraallee Intra osseous vertical plate of dense bone, located postero-medially at the neck shaft junction It is not the inferior cortex of the neck Function: buttress at the med neck & prox shaft to absorb most of WB compressive & bending forces It has 3 extensions (Harty 1957)

1]. Proximally ....................................................... extends to postero-inferior neck 2]. Laterally ........................................................... extends to GT anteriorly 3]. Distally............................................................... extends to LT postero-medially then fuse é the shaft

KKIINNEEMMAATTIICCSS

Motion Average range Flexion 115º Extension 30º Abduction 50º Adduction 30º Internal rotation 45º External rotation 45º

KKIINNEETTIICCSS • Joint Reaction force (JRF) is the force applied to the joint ð

internal and external factors • Wt is applied on lever arm passing from body centre to head

centre • Abductors act on a lever arm from the GT tip to head centre • The ratio of A:B = 1: 2.5 ∴ Abductors must work ≈ 2.5 BWt • Any disease head and neck length abd lever SSttaattiiccss Two leg stance • During a two leg stance the line of gravity of the body passes behind the pubic symphysis • As the hip joint is a stable joint, no muscle forces needed in stance • The force on each hip = ½ x (body wt – legs wt)

3 Single leg stance W is force produced by body weight; M is force produced by the abductors of the hip; R is the joint reaction force Assume A B and q are known For equilibrium Sum of moments = 0

• W x B=My x A • If B and A are known • My= W x B /A • A value for My is then found

For equilibrium Sum of the forces is 0 (in the Y axis) • My + W – Ry = 0 • Ry can therefore be found R can now be found by using • Ry =R sin q

On using elbows and heels to get onto a bed pan unaided • JRF at hip = 4 x body weight • Much reduced when using overhead trapeze

Using a walking stick how it reduces JRF: In equilibrium sum of moments = 0 Without Stick With Stick Ab x A = W x B (Ab x A) + (WS x C) = W x B Ab = W x B / A Ab = (W x B) –(WS x C) / A So the force required by the abductors Ab is smaller if a stick is used The bigger C is the smaller Ab, walking stick the furthest away from the hip the most effective In equilibrium, the sum of the forces in the Y plane = 0 Without stick With stick JRF sin q = Ab + W JRF sin q + WS = Ab + W JRF sin q = Ab + W – WS • Therefore JRF is less when a walking stick is used. Not only is Ab force smaller, but the upward

force exerted by the stick reduces the JRF further. • Body wt tend to push the stem into Varus and Retroversion: • Torsional stability by:

Longer neck cut Rounded rectangular cross section Cutting flutes Extensive porous coating

4 DYNAMICS

On walking Paul et al, using a force plate and kinematic data for the normal hip found 2 peaks in the Joint reaction force in the hip

Joint reaction force at just after heel strike JRF just before toe off Men 4 x body weight 7 x body weight Women 2.5 x body weight 4 x body weight

FFoorrcceess aaccttiinngg oonn tthhee hhiipp

1- Compressive forces: axial loads on the axis of the prosthesis 2- Bending forces: eccentric loads parallel to the axis of the prosthesis 3- Shear forces: forces applied é an angle to the axis of the prosthesis

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6 Nerve root innervation and function muscle action: muscles of the hip joint

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Osteonecrosis

DDeeffiinniittiioonn • = Death of bone from ischaemia. • Osteocytes will survive 12 - 48 hours of ischaemia and marrow cells 6 hours

FFeeaattuurreess • Age 20-50 y (average 38 y) ● ♂ > ♀ • Sites: in descending order

1- Femoral head 2- Medial femoral condyle 3- Humeral head 4- Talus 5- Lunate, proximal part of scaphoid 6- Capitellum 7- Metatarsal heads

• Bilateral in 50% of idiopathic cases, and 80% of steroid induced cases • 5% of THR performed as a result of OA secondary to AVN

PPaatthhooggeenneessiiss (Theories) 1. Direct injury: injury to retinacular vv in fr neck femur 2. Intraosseous Hypertension (Compartment Syndrome of Bone)

• Vascular sinusoid (no adventitia & éin a hard bone) can be compressed by surroundings

• IOP have been consistently found in cases of ON • IOP is inversely proportional to Bl flow ∴ IOP BF

ischaemia and ON 3. Vascular stasis

• Those sites are far distal, cartilage enclosed, & supplied é end art é insufficient collaterals

• Superselective angio of the medial circumflex a to study femoral head AVN

• Loss of transcortical blood flow from the superior retinacular have been demonstrated • revascularization occurs in non reversible osteonecrosis

4. Fat Embolism • subchondral fat volume vascular stasis platelet aggregation, hypercoagulability

& endothelial damage intravascular coagulation Θ local mechanisms of repair • Histologically: intraosseous thrombosis / peripheral haemorrhages.

5. Fat Cell Hypertrophy • high-dose corticosteroid Fat cell hypertrophy & fatty marrow overload • Histological changes consistent with necrosis were frequently identified and femoral head

blood flow was consistently diminished • Use of lipid clearing agents improve this alteration in blood flow.

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} Mottling

ÆÆttiioollooggyy:: 1. Idiopathic (40%) 2. Arterial insufficiency:

1. Fracture & Dislocation fr. neck femur, talus, scaphoid severe ! retinacular a 2. Infection

3. Arteriolar occlusion 1. Sickle cell disease and other haemoglobinopathies 2. Caisson disease in divers and compressed air workers (e.g. miners) 3. Vasculitis e.g. SLE, irradiation 4. Antiphospholipid $ (e.g. in SLE) 5. Coagulation disorders: thromobocytopenia, ITP, familial thrombophilia

4. Capillary occlusion (by fatty infilterates and swollen adipocytes) 1. Systemic steroid treatment (37%)

> 30 mg prednisolone for > 30 days 2. High alcohol intake (20%)

> 400 ml/wk or cumulative dose of 150 litres 3. Fatty liver ð other drugs e.g. chemotherapy 4. Gaucher’s disease 5. Hyperlipidaemia

5. Venous occlusion 6. Other

1. Pregnancy ( fibrinolysis, fatty liver) 2. Perthes’ 3. Pancreatitis 4. DM 5. IBS 6. Nephrotic $ 7. Renal transplant patients (16% will develop ON) 8. Haematological malignancies e.g. lymphomas, leukaemias 9. Toxic shock & endotoxin reactions

PPaatthhoollooggyy

• 6h ............................................Marrow cells can with stand iscemia • 12 - 48 h...................................Osteocytes can with stand iscemia

o Dead bone is grossly and radiologically look as normal bone for weeks • 2 - 4 d.......................................loss of BM adipocyte, oedema, infiltration, histeocytes

o Necrotic BM is replaced é UM tissue o Necrotic osteocytes may look normal for wks (Empty lacunae are a late feature)

• 2-4 weeks: ...............................necrotic sector becomes demarcated o substitution creeps from surviving trabeculae (10mm max).. rarefaction o New bone is laid down on the dead trabeculae ..................... sclerosis o Repair & revascularisation starts at vascular margin appositional growth

• Dead bone may fracture & collapse OR repair maintaining joint congruency • Shear stress + large + wt bearing lesion + inadequate remodelling tangential subchondral

stress fr & collapse • This fracture may run into the cartilage surface; that may resist breakage till it yields,

fragments, and leads to deformity & destruction of the joint surface • Necrotic segment never in size; even it may in size

11 CClliinniiccaallllyy:: early stage is asymptomatic and the pt present late

• Hip pain is common & present for months before X-Ray changes are manifest o Insidious pain ώ starts é activity or IR at rest eventually at night o Pain may be severe for 6-8 weeks and then subside o Night pain may be an early feature

• Clicking: due to snapping of loose fragment • Late deformity and stiffness • Mild symptoms and effusion usually persists • Earliest examination finding is IR • Late: tenderness, ROM, fixed deformity

IInnvveessttiiggaattiioonnss X-ray features

• S 0-I: NNOORRMMAALL • S II: Osteopenia (hyperaemia) & sclerosis (new bone) • S III: Subchondral CCOOLLLLAAPPSSEE “CCRREESSCCEENNTT sign” (sclerosis ) • S IV: 2ry OOAA joint space (before JS is normal)

MRI (100% sensitivity, 98% specificity) • Earliest finding (before gross and radiologic findings)

o T1: Bandlike area of low signal intensity ð ischaemic BM o T2: 2nd high signal intensity line éin the line seen on T1; hypervascular

granulation tissue “DDOOUUBBLLEE LLIINNEE SSIIGGNN” • When ¼ of head diameter & 2/3 of WB area is involved ⎯→⎯ %75

collapsed within 3y • Rarely AVN may be found on histology with a normal MRI • Small NWB lesions tend not to collapse • Size of ischemic segment is determined very early and rarely after that

MRI Staging for signals Class T1 T2 Definition A bright intermediate "fat" signal. B bright bright "blood" signal. C intermediate bright "fluid" or "edema" signal. D dark dark "fibrosis" signal.

Bone scan features 75-80% sensitivity in precollapse stage

• Tc99mSulphur colloid is taken by BM myeloid tissue; in AVN uptake • Tc99mHDP early (2-3wk) Cold area in blood phase (prior to revascularization hot) • Usually uptake at time of study • uptake on both sides of joint suggests OA rather than AVN

Single Photon Emission Computed Tomography (SPECT) scan • SPECT is a 3D isotope technique useful in analysis of BG healing & early AVN • It is able to visualize 3D bone reactivity identify cold spot éin area of activity

Hemodynamic Tests (bone marrow pressure) • Metaphyseal cannula is inserted and measure resting pressure and after rapid injection of saline • Three fold increase is noted (N: 10 mmHg rising to 15 mmHg) • This is also demonstrated by venography

Other investigations to diagnose the cause of the AVN • e.g. Alcohol abuse: γGt, urate, sTG, MCV • in non-traumatic and in Perthes’: coagulopathy profile is recommended • SLE & antiphospholipid $: antibodies are measured

T1 low signal band

T2 Double line

12 Staging

1- Ficat and Arlet Staging Stage Pain Findings X-ray Tc MRI Treatment 0 (Preclinical) None None (FEB +ve) N N +/- None I (Preradiological) Minimal IR N N +ve Core decomp II (Precollapse) Moderate ROM Osteopenia/

sclerosis +ve +ve Core decomp

Strut graft III Moderate/

Severe ROM Head collapse /

crescent sign +ve +ve Strut graft

THR IV Severe Pain 2ry OA +ve +ve THR

Original Ficat & Arlet 1968, did not include Stage 0. Stage 1 was known as the 'Silent Hip'. 2- Steinberg modification: same as above for stages 0-3 Stage IV Flattening of the femoral head Stage V Narrow Joint space ± acetabular involvement Stage VI OA Stages are further divided into:

A. Mild (A) B. Moderate (B) C. Severe (C)

3- Shimizu Predictive Staging (MRI staging) 4- Association Research Classification Osseous

13 FFuunnccttiioonnaall eexxpplloorraattiioonn ooff bboonnee ((FFEEBB)):: Simple and safe method for diagnosis in the early stages (pain / ROM / normal PXR) 1. Bone marrow pressure: BLP, ST, PO2

cannula placed in the intertrochanteric area under local anaesthesia “Base line pressure” N:20 mmHg; if IOP is normal 5 ml of isotonic saline is injected Pressure recorded 5 min after "stress test" pressure, is normally < 10 mmHg rise If both tests are normal repeated using a cannula placed in the head In AVN baseline pressure > 30 mmHg & stress test > 10 mmHg rise Blood sample from trochanteric area is taken for P.O2; if > 85% uptake = circulation failure = head anoxia

2. Intramedullary venography: • 10 ml contrast medium is injected through the same cannula used for the stress test • N: dye quickly cleared by ischial & circumflex veins, éout diaphyseal reflux or stasis • In AVN the injection is difficult/painful/diaphyseal reflux/IM stasis for 15 minutes • AVN diagnosis is probable even if only one of the BLP, ST, or venography is positive

3. Core biopsy • 3RD stage of FEB, establishes the diagnosis é certainty. • A trephine, 6 - 8 mm is introduced into the neck from an opening in GT head • Stop 5 mm subchondral under fluoroscopy • Second channel is made with a smaller trephine in a different direction • forage channels are left open, so providing decompression.

AArrlleett aanndd DDuurrrroouuxx HHiissttoollooggiiccaall ccllaassssiiffiiccaattiioonn Grade Pathology

GI haemopoietic marrow, odema, hemorrhage, foam cells GII marrow necrosis, eosinophilic reticular pattern, oil cysts GIII complete medullary and trabecular necrosis GVI complete necrosis + dense fibrosis + appositional new bone formation

DDDDxx ttrraannssiieenntt oosstteeooppoorroossiiss aanndd aavvaassccuullaarr nneeccrroossiiss ooff tthhee hhiipp

Avascular necrosis Transient osteoporosis Incidence 15,000 cases/yr Rare Patient

Male : female Equal 3 to 1 Age 20-40 years old ♂: 40 y; ♀ during last trimester of pregnancy In children Equivalent to Legg-Calvé-Perthes disease Extremely rare

PDF Known risk factors in 80 % of patients Pregnancy Etiology Interruption of circulation to femoral head Unknown; may be RSD or AVN Laterality Bilateral in more than 50% of patients Unilateral, may be recurrent Onset Insidious Acute Symptoms Pain at rest, limp (late finding) Pain é WB, antalgic gait, functional disability Imaging findings

PXR Osteopenia, Sclerosis, mottling, crescent, collapse Osteopenia at 4-6 wks. Bone

scanning Lesion more localized, may present with photopenic area

Diffuse, homogeneous lesion; increased uptake of isotope

MRI Focal lesion, anterosuperior region of femoral head; signal intensity on both T1- T2- double-line sign

Diffuse BM-edema pattern, Low signal on T1 High signal on T2

Prognosis Progressive in 70-80% of patients, usually leading to collapse of femoral head and end-stage degenerative joint disease

Spontaneously resolves within 6 to 8 mo without sequelae, prognosismore guarded in pregnant patients

Treatment Early operative intervention is recommended Protected weight-bearing & ttt of symptoms

14 TTrreeaattmmeenntt MMooddaalliittiieess • alcohol and steroids in high risk patients • Regulation of the rules for divers and air workers • Prevent anoxia for hemoglobinopathy patients • Arthrocentesis for traumatic hip tamponade • Potentially reversible early if corticosteroids or alcohol stopped • Antithrombothic medications in thrombophilia and hypofibrinolysis • Symptomatic treatment, weight loss and physio 1. Protective Weight bearing (Stage I & II) • Relative poor choice; however mb indicated in very limited disease or not fit for surgery • Start é NWB progress to FWB as clinically demonstrate that the hip is less irritable. • Usually it takes 3 - 6 months to return a patient to FWB status • Radiographic and clinical follow-up at 6-week intervals until pain has subsided • Success 5%-20% at 3-5 years (inferior to core decompression in Ficat stage I & II) 2. Core Decompression (Best for stage I & II) • Aim: demonstrate IOP (venous) remove a central core of bone IOP • The biopsy obtained can confirm the disease histologically • Patients remain NWB for 6 weeks post op • Meta-analysis of 24 studies involving 1206 hips treated with core decompression • Rates of preservation of the femoral head:

Core Decompression No Rx

Stage 1 84% 35% Stage 2 65% 31% Stage 3 47% 13%

Kaplan-Meier survival curves

Stage 5 yr 10 yr 15 yr No Further Surgery Needed 1 100% 96% 90% 88% 2 85% 74% 66% 72% 3 58% 35% 23% 26%

• Core decompression + PEMF results ~ the same as core decompression alone • Conclusion: Core decompression delays the need for THR

3. Electrical Stimulation (Stage I, II, III) • The use of PEMF’s with external coils in a large multicentre study was successful for

hips, irrespective of the aetiology of the condition. • As effective as core decompression for stages 1 and 2, but is more effective for stage 3 • Awaiting final FDA approval before it can become widely available

4. Trapdoor Procedure • Indicated for pre-collapse (Stage II) • Anterolateral dislocation of the head is done to expose the area of the collapse • The break in the articular cartilage is identified and opened like a trapdoor • Necrotic bone is excavated & removed if needed by burr expose bleeding bone • This defect is then filled with iliac BG overpacked to prevent subsidence • May cause subluxation; so it must be combined é acetabuloplasty ± VDO

15 5. Proximal Femoral Osteotomy (Stage III) • NB may compromise later THR • Aim is preservation of the head by stress in the diseased head sector. • Varus osteotomy shift the most involved portion medially (best for lateral lesions) • Success has been reported in 74% of stage 3 hips in one series • Rotational osteotomy (SSUUGGIIOOKKAA) shift the diseased portion med.inf.posterior

• It is technically difficult & associated é morbidity best reserved subchondral collapse • Its reported success rates are: Intact weight bearing area after transposition %Success > 60%, 100% > 36%, 93% 21% - 35% 65% < 20% 29%

6. Strut Grafting (Fibula/tibia/iliac crest) (Stage II pre-collapse) • Either Bonfiglio non-vascularized type or using a vascularised grafting technique • Effective if the graft is placed carefully in the subchondral region • Cortical strut grafts e.g. ilium, fibula placed into a core track in the femoral neck • Ineffective for stress-transfer in the upper femoral regions • Not widespread yet 7. Vascularised Pedicle Flaps • Quadratus femoris graft (Meters) - posterior • Tensor Fascia Lata muscle - anterior 8. Arthrodesis • Young patient with unilateral disease e.g. trauma • Problem is that 50-80% of cases are bilateral • Conclusion: best to manage conservatively until bad enough to perform THR 9. THR • Both uncemented and cemented total hip arthroplasty have been used in this population • Reported success rates are below what appear to be expected from series in other patient

populations

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Osteoarthritis

DDEEFFIINNIITTIIOONN Non-inflammatory degenerative joint disease ccc by progressive softening & disintegration of articular cartilage é associated new bone formation & capsular fibrosis

11.. It is not a simple wear as it is: asymmetrical, localized, & related to abnormal loading 22.. It is not purely degenerative (misnomer) as it is accompanied by a healing process in the

form of reactive new bone formation EEppiiddeemmiioollooggyy:: it is the commonest joint diseases and considered a universal disorder

• > 60y .....................................................50% 33.. Fingers, hip, knee, and spine are more affected than other sites 44.. OA hands are more common in females 55.. ♀:♂ = 2:1 (more DDH in ♀) unlike china & Africa

AAEETTIIOOLLOOGGYY • Primary - no obvious cause more é aging (effect of aging on cartilage) • Secondary - occurs following certain predisposing factors:

o Trauma: ......................................direct injury, deformity, joint instability o Congenital: ................................DDH, Perthes, Blount,…etc o Infection o Metabolic: ..................................ochronosis, hemochromatosis, gout, Paget o Endocrine disorder: ...................Acromegaly and hyperparathyroidism o Occupation: knee (in benders)- UL (vibrating tools) –hands (boxers) –shoulder

(pitchers) o Obesity: ...................................... loads across the WB joints

• OA is uncommon in pts é osteoporosis • OA is due to failure of chondrocytes to repair damaged cartilage. • There is a DDIISSPPAARRIITTYY BBEETT..SSTTRREESSSS AAPPPPLLIIEEDD AANNDD CCHHOONNDDRROOCCYYTTEE RREESSPPOONNSSEE. = 'wear vs. repair'

MMeecchhaanniiccaall ccaauusseess ooff tthhee ddiissppaarriittyy ooff tthhee ssttrreessss aanndd ssttrreennggtthh:: Abnormal Loads on normal joint:

• articular cartilage can withstand loads of up to 25MPa without damage. Loads exceeding this chondrocyte death & cartilage fissures.

• single impact loads or less intense multiple impact loads can cause articular damage. • impact loading loss of proteoglycans from matrix cartilage stiffness, hydraulic

permeability & disrupt collagen meshwork. • if repair cannot keep up with damage degeneration.

Normal load on abnormal Joints:

• Instability altered congruence shear & compression forces on regions of cart. • Partial loss of joint sensory innervation accelerates joint degeneration • Forced activity following joint injury or ACL transection joint degeneration, whereas

immobilisation after injury prevents degeneration.

17 PPAATTHHOOGGEENNEESSIISS

Theory 1 • The initiating event is FFAATTIIGGUUEE OOFF TTHHEE CCOOLLLLAAGGEENN MMEESSHHWWOORRKK HHYYDDRRAATTIIOONN of the

articular cartilage LLOOSSSS OOFF PPRROOTTEEOOGGLLYYCCAANNSS from the matrix into the synovial fluid • Cartilage SSOOFFTTEENN CCHHOONNDDRROOCCYYTTEESS DDIIEE release of proteolytic enz further damage • Cartilage deformation stresses on collagen network damage • Cartilage can’t withstand stresses ώ are concentrated on the subchondral bone

subchondral degeneration, cyst, vascularity, sclerosis • Repair occurs at the joint margin in the form of growth & endochondral ossification

hypertrophic osteophytes (unlike the atrophic diseases e.g. RA) • Evidence of collagenolytic activity; but collagen loss may be ð mechanical causes. Theory 2: • The initial lesions are SSUUBBCCHHOONNDDRRAALL MMIICCRROOFFRRAACCTTUURREESS following repetitive loading. • Healing of these microfractures undue subchondral bone & violation of Tide mark • A stress gradient develops articular cartilage is lost in areas of maximum stress • Underlying bone becomes hardened and eburnated • Proliferative changes also occur at the joint margins with formation of osteophytes.

MMoolleeccuullaarr PPaatthhoollooggyy::

1- WWAATTEERR content (unlike water content in ageing) – ð weakening of type 2 collagen 22-- PPRROOTTEEOOGGLLYYCCAANNSS ( size, chondroitin 6-sulphate, keratan sulphate, hyaluronic) 3- CCHHOONNDDRROOIITTIINN // KKEERRAATTIINN RRAATTIIOO (unlike ageing). 4- PPRROOTTEEOOGGLLYYCCAANN--DDEEGGRRAADDIINNGG EENNZZYYMMEESS (collagenase & stromelysin & plasmin) 5- collagen, and proteoglycans synthesis and loss net result level 6- Increased levels of:

o Matrix MMEETTAALLLLOOPPRROOTTEEIINNAASSEESS (MMPs) (collagenase, gelatinase, and stromelysin). oo CCAATTHHEEPPSSIINN BB & DD (proteases found in synovium, chondrocytes, and PNL) o IILL11 - enhances enzyme synthesis & has a catabolic effect. oo IILL66 oo TTNNFFαα oo TTGGFFββ o GAGs and polysulfuric acid

18 PPAATTHHOOLLOOGGYY • CCAARRTTIILLAAGGEE DDAAMMAAGGEE: (in pressure areas)

softening fibrillation (chondromalacia) cracks ulceration eburnation (loss of cartilage é sclerotic 'polished' bone) tufts of fibrocartilage on the bone surface

• OOSSTTEEOOPPHHYYTTEESS (in non-pressure areas) due to: vascularization of subchondral bone develop in the path of least resistance capsule traction & synovial metaplasia proliferation of cartilage adjacent to WB

area é endochondral ossification • Subchondral SSCCLLEERROOSSIISS, congestion, and IOP • Subchondral CCYYSSTTSS:

In the areas of max damage containing thick gelatinous material ð microfractures that degenerate & accumulate synovial fluid

• CCAAPPSSUULLAARR TTHHIICCKKEENNIINNGG and fibrosis deformity F AD IR (antero inferior capsule) • Mild SSYYNNOOVVIITTIISS usually (sometimes thick and villous) • FFRRAAGGMMEENNTTAATTIIOONN of osteochondral surfaces •• LLOOOOSSEE BBOODDIIEESS:: usually ð synovial metaplsia and extrusion and not separation of an osteophyte

MMiiccrroossccooppiiccaallllyy:: • Early:

Superficial SSPPLLIITTSS and irregularities Deep MMEETTAACCHHRROOMMAASSIIAA (depletion of matrix proteoglycans) CCHHOONNDDRROOCCYYTTEESS clusters SSUUBBCCHHOONNDDRRAALL OOSSTTEEOOBBLLAASSTTIICC activity, marked vascularity Margin OOSSTTEEOOPPHHYYTTEESS: ð cartilage hyperplasia and ossification

• Late: Extensive CCLLEEFFTTSS CCYYSSTTSS é amorphous material (squeezed synofluid, disintegrated trabeculae, osteonecrosis) Bone NNEECCRROOSSIISS and denuding

TTyyppeess 1. Hypertrophic 75% 2. Atrophic 20% 3. Progressive 5%

VVaarriiaannttss:: 1. Polyarticular (generalized): commonest, 50y♀, hands painful stiffness, also trapMC OA 2. Monoarticular & Pauciarticular: is the classic form, WB OA or 2ry to a cause (DDH) 3. Endemic OA: either environmental factor or genetic dysplasia 4. Unusual site OA: Milwaukee shoulder 5. kashin-Beck disease: generalized OA in hands, elbows, knees + short stature 6. Mseleni joint disease: Polyarticular esp hips crippling deformities ð MED & protrusio 7. Rapid destructive OA: elder ♂ under strong NSAIDs, usually hip ð Ca2+ crystal deposition 8. Charcot’s disease: the most severe form of OA

19 CCPP • Old age, +ve family history, + PF • WB joints (hands in females) • Insidious onset & Intermittent course é attacks may lasts for few months

1. PPAAIINN: 1- The main symptom: ð ms fatigue, capsular stretch, congestion, IOP 2- Site: anterior (sometimes posterior or lateral) 3- é exertion, WB, Cold, Ext Abd IR 4- é rest (relief by time) 5- Referred to medial side of the knee (via the obturator n.) 6- Progress to be even at rest

2. SSTTIIFFFFNNEESSSS & loss of function: after periods of inactivity ⎯⎯→⎯Later constant 3. DDEEFFOORRMMIITTYY: FF AAdddd EERR ; ð ms spasm ⎯⎯→⎯Later capsular contracture 4. RROOMM ± crepitus (especially Ext Abd IR) 5. Ms WWAASSTTIINNGG: in acute stage mainly in the abductors 66.. TTEENNDDEERRNNEESSSS:: over the site of capsular inflammation (most accessible bet. GT & ischium) 7. SSWWEELLLLIINNGG: intermittent (effusion) or constant (cap/synovial thickening, or osteophytes) 8. ++VVEE FF AABB EERR test: abduction Ext.rotation in flexion pain

• HHEEBBEERRDDEENN’’SS NNOODDEESS: thickening of the DIP joints (≠ Bouchard’s nodes of RA) RRaaddiiooggrraapphhyy • PXR:

1- Asymmetrical narrowing of joint space 2- Subchondral sclerosis 3- Subchondral cysts 4- Osteophytes at the margins 5- Late bone destruction and joint deformity and instability

• Tc-HDP scan uptake in bone phase ( vascularity & new bone formation)

CCOOMMPPLLIICCAATTIIOONNSS 1- Loose bodies 2- Backer’s cyst: capsular herniation 3- Spinal deformity 2ry to pelvic deformity lordosis & side bend 4- Ankylosis

TTRREEAATTMMEENNTT:: Vary according to the site, stage, age, severity, and symptoms • Early: keep moving, prevent overload, relieve pain,

1. EEXXEERRCCIISSEE of supporting muscles around joints to avoid wasting and keep ROM 2. PPRROOTTEECCTTIIOONN of affected joints from overloading: wt, walking stick 3. Pain relief by analgesics or NNSSAAIIDDSS. 4. MMOODDIIFFYY activity: avoid climbing stairs, squatting,… etc 5. HHYYAALLUURROONNIICC acid injections 6. GGLLUUCCOOSSAAMMIINNEE & chondroitin

• New & Experimental Treatments: 1. Doxycycline Θ cartilage collagenase activity 2. Transforming growth factor beta (TGF beta) can repair partial thickness lesions 3. Metalloproteinase inhibitors Θ matrix destroying enzymes & block cytokines 4. Gene therapy - Genes that have either anti-arthritic or synthetic properties can be

delivered into the joint via non-replicating viral vectors; e.g. IL1

} + any other 1ry pathology

20 • Late Surgical treatment - is indicated for patients é persistent symptoms: 1- Cysts curette and BG release the fluid under pressure inside (obsolete) 2- BG of AVN (to be effective must be precollapse) 3- Arthroscopic debridement, wash, removal of LBs, and removal of osteophytes 4- RREEAALLIIGGNNMMEENNTT OOSSTTEEOOTTOOMMIIEESS in young age;

Advantages: 1- pain ð:

Unload the disease part decompress the congested metaphysis relief pain dramatically adduction of prox fragment relax ! capsule & Intraarticular tension Relax the adductors

2- joint space 3- cysts and sclerosis

Indications of valgus osteotomies: 1- Fixed adduction deformity 2- Painful abduction 3- Trendelenberg gait 4- Must have adduction range after the osteotomy

Indications of varus osteotomies: 1- Fixed Abduction deformity 2- Painful adduction 3- Antalgic abductor gait 4- Must have abduction range after the osteotomy (confirm by PXR)

Contraindications: 1- Extensive OA é ROM < 50º 2- RA 3- Extensive AVN é no healthy segment to be utilized for WB

Precautions: 1- Pre PXR in adduction and abduction to determine the osteotomy

angle 2- Never do varus osteotomy for varus deformity and Vice versa 3- stable internal fixation is mandatory

5- HHAANNGGIINNGG HHIIPP OOPPEERRAATTIIOONN: muscle release all around the hip via 3 incisions to joint tension and regain attachment é elongation after few weeks (obsolete)

6- AARRTTHHRROODDEESSIISS if young and stiffness is accepted Indications:

1- Severe unilateral OA 2- Severe limitation of movements 3- Medical treatment is exhausted 4- Epsilateral knee & spine should be sound

7- GGIIRRDDLLEE SSTTOONNEE:: may be done after failure or sepsis of arthroplasty as a transition till 2nd op 8- PPEELLVVIICC SSUUPPPPOORRTT OOSSTTEEOOTTOOMMYY: Girdle stone + subtrochanteric osteotomy at the level of the

ischium é angulation beneath the acetabulum for WB support; it provides support, pain relief, motion especially in chronic infection, OA after infection & Unreduced DDH

9- CCOOLLOONNNNAA TTRROOCCHHAANNTTEERRIICC RREECCOONNSSTTRRUUCCTTIIOONN: resection of head and neck + implantation of the GT into the acetabulum

10- AARRTTHHRROOPPLLAASSTTIIEESS;; (Total, femoral head, cup) for old patients (>60y) in advanced cases

21

TB Hip • Tuberculosis is common throughout the world •• Usually due to Mycobacterium tuberculosis or Mycobacterium bovis infection

PPaatthhoollooggyy:: 1. 1ry lesion:

• Site: o Lung usually (sub-pleural Ghon’s Focus and mediastinal

lymphadenopathy) o Pharynx ▪ Gut

• Changes: o Local inflammatory focus Lymphangitis Lymphadenitis

• Seculae: o TB bacilli remain dormant in LN (intra macrophage) o Body is sensitized to toxin (Type IV cell mediated delayed hypersensitivity)

2. 2ry lesion: • Due to reactivation, repeat exposure, immunity (e.g. drugs or HIV infection) • Results in more significant symptoms as it spreads to:

o Lung .................... military TB, TB bronchopeumonia o Meninges:............. TB meningitis

3. 3ry lesions (10% affect the musculoskeletal system) 11.. Tuberculoma formation:

o Central CCAASSEEAATTIIOONN necrosis (coagulation necrosis) o Surrounded by EEPPIITTHHEELLIIOOIIDD cells, LLAANNGGEERRHHAANNSS giant cells, LLYYMMPPHHOOCCYYTTEESS o They tend to coalesce to form a wide area of caseation necrosis o Spread to cartilage destruction and spread to joint space

22.. TB Spondylitis: (mainly throracic) o Starts in ant. body at multiple level; destroy bone & respect ! disc except late o PPOOTTTT’’SS PPAARRAAPPLLEEGGIIAA ð (kyphosis, abscess, blood supply to the cord)

33.. Tb Arthritis (hip, knee, ankle, shoulder, then wrist) o Synovium is TTHHIICCKKEENNEEDD é Cell rich EEFFFFUUSSIIOONN o Granulomatous PPAANNNNUUSS may form & creaps on the cartilage & bone o Cartilage & bone EERROOSSIIOONN (peripherally at synovial reflection) o Juxta articular OOSSTTEEOOPPEENNIIAA ð hyperaemia

44.. Appendicular skeleton: o Metaphyseal bone destruction (no sclerosis, no periosteal reaction)

55.. TB Dactylitis = Spina Ventosa (middle and distal phalanx) o Digit is swollen spindle shape é little pain o Starts diaphyseal é bone rarefaction + PNBF + soft tissue swelling o PXR: Spina (spindle shaped digit) Ventosa (full of are i.e. rarefied)

66.. Cold Abscess: o Infected LN may CCOOAALLAASSEE together to form big area of caseation o Caseation spread via soft tissue planes o May burst to skin to form a sinus o May collect at a distant site far from original pathology e.g lumbar TB

groin 4. Healing:

11.. Resolution 22.. Fibrous Ankylosis 33.. Dormant bacilli

22 CClliinniiccaallllyy::

General: • Night sweat, night fever • Loss of weight, loss of appetite

Local: • NNIIGGHHTT CCRRIIEESS: joint is splinted at day time by spastic ms ⎯⎯ →⎯AtNight spasm is relieved

stretch or compression of the damaged tissue pain • Marked MMSS WWAASSTTIINNGG • Marked SSYYNNOOVVIIAALL TTHHIICCKKEENNIINNGG • ROM & SSTTIIFFFFNNEESSSS • Joint DDEEFFOORRMMIITTYY 1st FF AABB EERR (with effusion) ⎯⎯→⎯Then FF AABB IIRR (destruction of the joint) • Spine: pain, abscess kyphosis, neurological manifestation

PPXXRR:: • JJUUXXTTAA AARRTTIICCUULLAARR OOSSTTEEOOPPEENNIIAA washed out bone ends • JJOOIINNTT SSPPAACCEE (in children epiphysis 2ry to hyperaemia) • Peripheral bone EERROOSSIIOONN and CCYYSSTTIICC subchondral lesions • NNOO PPEERRIIOOSSTTEEAALL reaction •• NNOO SSCCLLEERROOSSIISS •• Spine erosion, collapse, paraspinal abscess calcification & kyphosis é crowded

related ribs SSUUNN RRAAYY AAPPPPEEAARRAANNCCEE • Hip erosions occur in 3 areas; superior acetabular rim, GT, & BBAABBCCOOCCKK’’SS Δ;

erosion of the superior acetabulum WWAANNDDEERRIINNGG AACCEETTAABBUULLUUMM IInnvveessttiiggaattiioonn

• ESR • Leucopenia é relative lymphocytosis • Lymphocyte/monocyte ratio may reach 1 • +ve Mantoux test (indicate TB infection recent or old) • +Ve PCR • Synovial fluid:

1. ptn, glucose 2. viscosity, poor mucin clot 3. Red acid-alcohol fast IINNTTRRAACCEELLLLUULLAARR bacilli é ZZEEAALL NNEELLSSEENN....20% 4. Cultivation on LLOOWWEENNSSTTEEIINN JJEENNSSEENN media or Dorset egg ........80%

1. Difficult to culture needs adequate relevant conc. (centrifuged) sample 2. Decontaminate & remove other organism (Petroff method) 3. Keep 35º for 6 wk

5. Organisms also FFLLUUOORREESSCCEE WWIITTHH AAUURRAAMMIINNEE staining 6. Negative microscopy does not exclude tuberculosis 7. Guinea pig inoculation

• Synovial biopsy: 1- Granulomatous reaction (central caseation + Langerhans + epitheliod +

lymphocytes) 2- Characteristic evidence of a delayed hypersensitivity reaction

} PPHHEEMMIISSTTEERR Triad

23 SSkkiinn tteessttss

• Delayed hypersensitivity reaction used to diagnose tuberculosis • The two commonest tests are the Mantoux and Heaf test • Mantoux test:

0.1 ml of purified protein derivative is injected intradermally +ve if ...................................> 5 mm papule at 72 hours

• Heaf test PPD is inoculated into the skin using a gun to produce multiple punctures +ve if ...................................> 4 papules at puncture sites at 72 hours

• Positive skin test are indicative of active infection or previous BCG vaccination DDDDxx

1- Transient synovitis 2- Monarticular RA 3- Subacute arthritis 4- Old septic arthritis

TTrreeaattmmeenntt

Rest: Splintage and traction to prevent ms spasm and deformity Maintained till pain and inflammation is over Then motion is encouraged; if pain & spasm return, resume splints (Thomas

2nd Test) Chemotherapy:

RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin Rifampicin + Isoniazid 6-8 mo Ethambutol (or pyrazinamide, spectinomycin) for the initial 8wk Streptomycin is toxic

When to start surgical ttt: Clinically: ................................................ No fever, no wt loss, no spasm PXR: ....................................................... calcification Lab: ................................................................ ESR, lymph/monocyte ratio >5

Operative: Drainge of a TB focus is seldom done nowadays Cold abscess .................................................. calls for urgent drainage GT bursitis ....................................................Bursectomy Young age...................................................... synovectomy Clearance operation.......................................debride all infected & dead tissue Painful destroyed joint in middle age........... arthrodesis instead of painful fibrous

ankylosis Painful destroyed joint .............................. Girdle stone then arthroplasty

24

Synovium

= inner lining of synovial joints • Synovial membrane is not a true membrane since it does not have cells joined to their neighbours by tight

junctions (desmosomes) and has no basement membrane of collagen. • Instead the cells are loosely arranged on a matrix of hyluronate (secreted by the synovial B cells). • It is one or two layers thick • Supported by capillaries & thin fibrous stroma • Richly supplied with blood vessels, lymphatics, and nerves; richness of blood capillaries and their

proximity to inner surface account for hemorrhage into joints that may follow minor injuries Cells:

• A Cells = macrophages • B Cells

o exocrine / synthetic cells o synthesize hyaluronic & glycosaminoglycan (GAG)

• C Cells May exist as an intermediate cell type. • Arranged into microvilli & villi resulting in a large surface area

(knee = 100m2; whole body = 1000m2) Functions of Synovium

1. Controls diffusion 2. Ingest debris 3. secrete immunoglobulins 4. secrete lysosomal enzymes 5. secrete hyaluronate & glycoproteins 6. reduce friction in joint

Regenerative Capacity

• synovial cells may transform into chondrocytes at attachment site of Synovium to articular cartilage • synovial cells are capable of rapid and complete repair or regeneration

Response to Infection: 1- Acute inflammatory response with accumulation of PMN's & monocytes 2- complement activation produces chemotactic factors and other inflammatory mediators 3- lysosomal enzymes attack hyaluronate leading to loss of the diffusion barrier 4- inflamed synovium contains large clefts which probably permit passage of molecules of almost any size 5- synovium becomes a 'leaky sieve' 6- if infection is not ttt synovium necroses éin 24H chondrocytes necrosis & failure of GAG production 7- acute inflammatory response along with cellular disintegration (with release of lysosomal enzymes &

proteases) will further injure chondrocytes 8- Antibiotics can also easily get into the joint 9- Lysosomal enzymes (collagenase, protease, galactosidase) damage the joint joint toilette required 10- Hydrocortisone blocks the release of lysosomal enzymes

SYNOVIAL FLUID = an ultrafiltrate of blood plasma (by molecular sieving) plus hyaluronic & glycoproteins The viscosity depends on amount of hyaluronate. Does not contain fibrinogen - thus no clotting Exhibits non-newtonian fluid characteristics - viscosity é shear rate. Functions:

• Nourishes articular cartilage through diffusion • Lubricates via the following mechanisms:

o Hydrodnamic (fluid seperates the surfaces under load) o Boundary (slippery surfaces) o Weeping (fluid shifted to loaded areas) o Boosted (fluid entrapment)

Lubricin (a glycoprotein) is a key lubricating component DISEASES OF SYNOVIUM

1]. Pigmented Villonodular Synovitis (PVNS) 2]. Rheumatoid Arthritis 3]. Synovial Chondromatosis

25

Rheumatoid Arthritis • Affects 3% of women & 1% of men • Hand > Knee > hip > cervical spine

DDiiaaggnnoossiiss:: • ARA Criteria (American Rheumatism Association):

1- Morning stiffness Lasting at least 1 hour before maximal improvement.

2- Arthritis of 3 or more joint areas At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony overgrowth alone) observed by a physician; the 14 possible joint areas are right or left proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, wrist, elbow, knee, ankle, and metatarsophalangeal (MTP) joints. 3- Arthritis of hand joints

At least 1 area swollen (as defined above) in a wrist, MCP or PIP joint. 4- Symmetric arthritis 5- Rheumatoid nodules

Over bony prominences, or extensor surfaces, or in juxta-articular regions 6- Rheumatoid factor +ve 7- Radiographic changes

• At least 4 of 7 criteria. • Criteria 1 through 4 (at least 6 weeks). • Clinical Staging:

o 7 ccc ........................................Classic o 5 ccc ........................................Definite o 3 ccc ........................................Probable o 2 ccc ........................................Possible

AAeettiioollooggyy::

• Genetic susceptibility: RA is common in first degree relatives of RA patients and twins

• Immunological process: HLA-DR4 & DW4 encoded on chromosome 6; and is found on the surface of APC (antigen presenting cells); & when interact é the antigen (some times the antigen with the HLA form the activating complex) autoimmune response

• When APC and T-cells interact cell proliferation + cyokines secretion ⊕ phagocytes & B-cells

• Rheumatoid factor: Anti-IgG auto antibodies which is detected in the serum of the patient

26 PPaatthhoollooggyy::

Stage 1: Synovitis • vascular congestion & effusion • synoviocyte proliferation VVIILLLLOOUUSS formation • infiltration of subsynovial layers by PMNs, lymphocytes & plasma cells

Stage 2: Destruction • a PPAANNNNUUSS of granulation tissue creeps over the articular surface eroding cartilage & bone • cartilage destruction occur partly ð proteolytic enzymes & vascular tissue • bone destruction occur partly by proteolytic enz, & osteoclastic activity • direct invasion occurs at the margins of the joint • similar changes occur in tendon sheaths rupture

Stage 3: Deformity: • From:

a. articular destruction b. capsular stretching c. tendon ruptures

• acute inflammation subsided

EExxttrraa--aarrttiiccuullaarr MMaanniiffeessttaattiioonnss:: • Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera • Lymphadenopathy & Splenomegaly ....... FFEELLTTYY''SS Syndrome (pancytopenia) • salivary & lacrimal gland secretion ..... SSJJOORRGGEENN Syndrome • Pulmonary (pleurisy & rh nodules) ......... CCAAPPLLAANN $ • Vasculitis • Myopathy & neuropathy, or direct compression from synovitis • Visceral: pericarditis, nodules

CClliinniiccaallllyy:: • 40 female may be é positive family history • Early:

Painful swollen HHAANNDD joints é morning stiffness PPAAIINNFFUULL LLIIMMPPIINNGG RROOMM ± crepitus (especially Ext Abd IR) loss of WWEEIIGGHHTT, weakness O/E: symmetrical swelling, tenderness, crepitation, synovial hypertrophy

• Late: DDEEFFOORRMMIITTYY: F Add ER Instability, tendon rupture PPAATTHH ##:: from the disease and drugs (usually neck femur) BBOOUUCCHHAARRDD’’SS nodules, Swan neck , Boutonniere, Z-thumb, fingers ulnar

deviation, wrist radio-volar deviation, valgus knee, valgus feet, clawed toes, atlanto-axial subluxation

• Types of presentations: Palendromic: starts intermittent episodes of multi joint affection evolve to

classic Systemic: severe form é visceral affection Monoarticular: usually knee. Also, may present as tenosynovitis or CT$ Myalgic: as fibromyalgia rheumatica but with +ve RF

27 LLaabboorraattoorryy FFiinnddiinnggss::

• . ESR, CRP • RF +ve in 80%, ANA 30% • ACCP (anti Cyclic Cetrolinated Peptide): 97% early +ve in RA even in seronegative RA • anemia: ð abnormal erythropoiesis, and chronic blood loss from analgesic gastritis • WBC: Normal or (if suspect Felty) • Complement

Synovial biopsy & fluid: • Biopsy: is non specific to RA • Fluid: ptn, C, glucose / poor clot / RA cells & PNL

PPXXRR:: LLAARRSSEENN == DDAALLEE RRAADDIIOOLLOOGGIICC IINNDDEEXX 1- Stage I: juxta-articular osteopenia 2- Stage II: Narrow joint space (usually bilateral, symmetrical, concentric ± protrosio) 3- Stage III: Bone erosion of the head near the neck + bone cysts 4- Stage IV: Deformity (don’t forget the cervical PXR) • Usually no sclerosis nor osteophytes (except if 2ry OA) • Other complications: AVN, fracture neck

DDDDxx:: 1- Seronegative: SLE, Still’s 2- AS: spondarthropathy 3- Reiter’s: Conjunctivits, urethritis, Arthritis 4- Gout & CPPD: crystals 5- OA: DIP affection, osteophytes 6- Polymyalgia rheumatica: pelvic, and pectoral weakness, and aching, +ve steroid test 7- Sarcoidosis: Erythema nodosum, Hilar LN, +ve Kveim test

MMaannaaggeemmeenntt PPrriinncciipplleess::

• Stop the Synovitis o Rest o DMAR Drugs (Disease Modifying Anti-Rheumatic) - Pyramid Approach =

NSAIDs - antimalarials - sulphasalazine – gold – MTX – D-penicillamine - Azathioprine – Leflunomide + low dose steroids

o Synovectomy - chemical, irradiation, surgical • Prevent Deformity

o Splintage o Physiotherapy o Tendon repairs & joint stabilisation

• Reconstruct (start é knee if > 45º flexion deformity) o Arthroplasty is the gold standard o Osteotomy not done:

Doesn’t remove the cartilage ώ is a source of inflammation

RA is concentric & no healthy cartilage o Arthrodesis not to be done (bilateral)

• Rehabilitate & keep moving o Occupational therapists - aids, support o Physiotherapy

28

At Onset: NSAID, exercise Early: NSAID, Steroids, DMD, local injections, physiotherapy, Rest and splitage Erosive: DMD, splintage, operative (synovectomy, tendon repair, joint stabilization) Late Reconstructive arthroplasty PPrroobblleemmss éé ssuurrggeerryy::

1- Bilateral hip involvement 2- Ipsilateral knee involvement.........................needed for ambulation; if flexion def >45º start é it 3- UL affection ..................................................needed for PWB 4- Infections ......................................................scan for oral, UTI, skin before surgery 5- Bad general condition & systemic disease 6- Cortisone therapy .........................................need to the dose preop 7- Atlantoaxial subluxation ..............................difficult intubation 8- Protrusio acetabuli ........................................manage 9- Femoral #s ....................................................be gentle & ready 10- Loosening .....................................................Cemented or Hybrid are favored

Drugs Details:

Drug Mechanism A/E NSAIDs Θ PG synthesis pain and inflammation Gastric Upset Antimalaria Θ PG & phagocytic activity of PNL Lucoma Sulphaslsazine Anti-inflammatory Megaloblastic anemia Gold Alters the function of macrophages and complement Thrombocytopenia Methotrexate Immune suppression Liver toxicity D-Penicillamine Dissolve RF complexes in joints to be excreted Late resp.& nephrotic Azathioprine Immuno suppression Liver toxicity Leflunomide Θ DiHydro-Orotate Dehydrogenase T-cell prolif

Complications: • Fixed Deformities • Joint Rupture • Infection • Spinal cord compression • PN compression • Vasculitis • Amyloidosis, proteinuria • progressive RF

Poor prognostic signs: • Very high RF • Peri-articular erosions • Nodules • Muscle wasting • Joint contractures • Vasculitis

Prognosis: • 10% improve after first attack of synovitis • 60% have remissions & exacerbations • 20% have severe joint erosions requiring multiple operations • 10% become completely disabled

29

30

Prutrosio Acetabuli ÆÆttiioollooggyy::

I]. Idiopathic (young female bilateral)= Otto pelvis = AARRTTHHRROOKKAATTAADDYYSSIISS II]. 2ry:

1]. Congenital: Marfan syndrome 2]. Tauma 3]. Infection 4]. Inflammatory:

RA Ankylosing spondylitis

5]. Metabolic bone disease: Osteomalacia & Rickets Osteoporosis Paget’s disease

PPaatthhoollooggyy:: • Probably it results from remodeling of a weak medial wall after repeated stress #s • In 1ry cases medial displacement continue till the GT impinge on the acetabular rim otto

stops and the ossification of the medial wall begins (N.B. healing ώ is rare in 2ry prutrosio)

CClliinniiccaallllyy:: ...................................................Usually asymptomatic • PPAAIINNFFUULL LLIIMMPP as OA develops • RROOMM especially abduction • FFLLEEXXIIOONN DDEEFFOORRMMIITTYY lordosis • PR examination lateral globular mass over the rectal wall

RRaaddiioollooggiiccaallllyy:: 1]. Medial intrapelvic bluge of the acetabulum ± head erosion 2]. WWIIBBEERRGG CCEE angle > 40º 3]. AALLTTEERREEDD TTEEAARR DDRROOPP (formed of medial acet wall & quadrilateral plate) 4]. BBRROOKKEENN KKÖÖHHLLEERR line (ilioischial line); >1-3mm in ♂ / >3-6mm in ♀

RRAAMMOOSS ♂♂mm ♀♀ CCHHAARRNNEELLYY && GGAARRZZAA OOVVEERRGGAAAARRDD (tear drop) Mild <8 <11 <5mm Closed Moderate 9-12 12-17 6-15 Crossed Severe >13 >17 >15 Reversed

5]. BBRROOKKEENN IILLIIOOPPEECCTTIINNEEAALL line 6]. RRAANNAAWWAATT :

a. Pelvic height = the ⊥ distance bet the 2 parallel horizontal lines drawn at the levels of the ischial tuberosities and the iliac crests.

b. Point (1) located 5 mm med to the intersection between Shenton’s (5) and Kohler’s (4) c. Point (2) is located above point 1, at a distance = 1/5 of the pelvic height d. Point (3) is located medial to point (2) by the same distance bet 1 & 2. e. The isosceles bet 1, 2, 3 locates the normal acetabulum, é the line 2-3 being the sourcil

TTrreeaattmmeenntt • Conservative:

1. Protective WB 2. Steroid, NSAIDs, heat 3. ttt the cause

• Surgical: If advanced OA or progressive (1ry) 4. Valgus trochanteric osteotomy: pain & progression only; but does not ROM 5. Cup arthroplasty: temporary and needs thick medial wall 6. Arthrodesis: in young unilateral cases 7. Bone Transplantation: bone graft is fixed to the floor of the acetabulum till THR 8. Wire mesh: placed over the transplanted BG 9. THR

31

Transient Synovitis Of The Hip

• It is the most common cause of hip pain in children 2-12y • More common in males

ÆÆttiioollooggyy 1]. Viral infection: (usually preceded by sore throat) 2]. Allergic hypersensitivity to septic focus in the body 3]. Trauma

CClliinniiccaallllyy • Normal temprature • Acute PPAAIINN radiating to the knee and ant thigh • LLIIMMPPIINNGG ± inability to WB • RROOMM especially (Abduction IR) • Ms SSPPAASSMM (flexors and adductors) • Local TTEENNDDEERRNNEESSSS

PPXXRR 1]. NAD 2]. ± joint space 3]. ± LLAATTEERRAALL HHEEAADD DDIISSPPLLAACCEEMMEENNTT < 2mm (if > 4mm suspect PPEERRTTHHEESS’’)

UUSS • Effusion and thick capsule • Aspirate the effusion to exclude septic artheitis

TTcc • Only to role out Perthes’

LLaabb • Normal WBC • ESR • -ve culture

DDDDxx • By exclusion of Perthes’, TB, Septic, RA

TTrreeaattmmeenntt • Bed rest + light traction usually complete recovery in most of the cases • If severe symptoms & effusion on US aspirate the effusion for relief and to avoid AVN • Once ms spasm disappeared AROM & PWB • Follow up to 3mo by US & PXR if persistent lateral displacement Abduction splint even if

there is no evidence of Perthes’

CCAALLCCIIFFIIEEDD TTEENNDDOONNIITTIISS OOFF TTHHEE HHIIPP • Amorphous Ca deposition in the tendon of:

o Gluteus medius lateral to the GT o Gluteus minimus superior to the capsule of the hip joint

CClliinniiccaallllyy:: • Painful Limping • Ms spasm

PPXXRR:: • cloudy opacity on the soft tissue

tttttt:: • Heat & rest & NSAID if persists excision

32

Coxa Saltans SSNNAAPPPPIINNGG HHIIPP

• Audible and felt or even visible snap made when a tense fascial band catches as it slides over the superior margin of the GT as the hip is flexed add or IR

ÆÆttiioollooggyy 1]. External...................................GT é soft tissue around 2]. Internal....................................Iliopsoas tendon é the structures behind it (e.g. bursa) 3]. Intra articular ........................ Synovial chondromatosis Loose bodies Labral tears or fracture fragments

PPaatthhoollooggyy (of external) • The band consist of the thickened posterior border of the ITB • Anterior border of the gluteus maximus near its insertion

CClliinniiccaallllyy • The snap can be produced voluntarily and painless • Involuntary, painful, and habitual

TTrreeaattmmeenntt 1]. External...................................Z-plasty of the ITB é local anaesthesia PWB and wide gait 6wk 2]. Internal ...................................Z-Plasty of the ilio psoas tendon 3]. Intraarticular ........................ttt the cause

Hip Bursitis IInnttrroodduuccttiioonn

• 18 bursae are found around the hip • Only 3 are important: trochanteric, iliopectineal, ischiogluteal • Bursitis are usually due to over use & excessive pressure & subsides é rest, heat

IInntteerrttrroocchhaanntteerriicc BBuurrssaa • Between the GT and the gluteus maximus • Pain é flexion IR • ttt: if septic excision & drainage

IIlliiooppeeccttiinneeaall BBuurrssaa • it is the largest bursa around the hip & 10% communicate é the hip joint • between the iliopsoas and the iliopectineal eminence 1]. Pain & tenderness over the femoral 2]. Pain may radiate along the femoral n. to the anterior aspect of the thigh 3]. Coxa saltans

IIsscchhiioo--GGlluutteeaall bbuurrssaa • Over the ischeal tuberosity • Inflamed in occupations é prolonged sitting (e.g. tailors) • May produce sciatica • ttt: avoid prolonged sitting or excision

33

Proximal Femoral & Pelvic Osteotomies • The aim of an osteotomy is to realign the weight bearing surfaces of the joint to allow normal

areas to articulate, moving the abnormal area away from the weight bearing axis. • = reduce point loading & improve congruity. • This can be achieved by either performing a proximal femoral or pelvic osteotomy (or both) • Proximal femoral osteotomy blood flow to the femoral head & neck & venous drainage. • For early disease results of 80-90% relief of pain. • Success rates = 70% over 11 years follow-up • However, conversion to THR can be difficult due to alignment of femur & metalwork which can

be difficult to remove. IInnddiiccaattiioonnss

1. Reserved for young patients with advanced degenerative changes in whom THR is not wise 2. Non-union of a femoral neck fracture 3. Dysplasia (varus osteotomy) 4. Post-Perthes hinge abduction (valgus extension osteotomy) 5. SCFE (flexion osteotomy) 6. AVN (flexion osteotomy) 7. Idiopathic protrusio (valgus extension osteotomy)

CClliinniiccaall • Pain in certain hip positions only (e.g. adduction WBing) • Arc of Movement - which part of the arc is painful • Leg lengths (effect of FFD)

PPllaannnniinngg • Careful pre-operative planning required to find the position of the LLEEAASSTT PPAAIINN && CCOONNGGRRUUEENNTT • For varus osteotomy must have >>1155ºº AABBDDUUCCTTIIOONN preop. • For Valgus osteotomy must have >>1155ºº AADDDDUUCCTTIIOONN preop. • AP and lateral X-rays are taken in adduction/abduction • BBEERRNNEE or FFAAUUXX PPRROOFFIILLEE view (WB + 25º body tilt) - shows anterior uncovering. • CT or MR can give additional information • Best results are in young, non obese patients with a good range of motion (minimum 90º

flexion, 15º abduction/adduction) • Femoral osteotomy may distort the anatomy which may jeopardise a future THR • Need to determine:

1. The amount & direction of correction 2. choice of implant

VVaarruuss OOsstteeoottoommyy • generally indicated where lateral subluxation is associated with coxa valga. • Require good range of abduction prior to surgery. • Relaxes adductors, abductors & flexors. • Disadv- shortens leg. • must have >15deg. abduction preop

VVaallgguuss OOsstteeoottoommyy • Indic:

1. uncovered head made worse by abducting hip 2. deformed head with lateral osteophyte (post Perthes) 3. fixed adduction deformity

• Can add lat displacement of GT to hip joint reaction forces • must have >15deg. adduction preop.

CCoonnttrraaiinnddiiccaattiioonnss:: 1. Stiff 2. Obese 3. Gross narrowing with sclerosis & no normal joint surface 4. Atrophic inflammatory features