Arthroplasty Flashcards
Vancouver Classification for periprosthetic THA and Tx?
A: troch fx, if less than 2 cm displacement can tx nonop
B1: Stable stem, ORIF with locking plate and cables
B2: loose stem, long porous coated or MFTS
B3: poor bone stock and loose, Femoral revision with proximal femoral allograft or PFR
C: Fx well below prosthesis, ORIF with plate
Risk factor for intraop femoral fx during THA?
Female*** Anterolateral approach**** (vs posterolateral) MIS surgery Cementless stem*** Revision*** Metabolic bone disease***
Intraop calcar fx treated with cerclage does NOT increase risk of component subsidence or failure in long term f/u
Polyethylene sterilization
1-Radiation, oxidation vs cross linking, removal of free radicals
2 - how to solve these issues?
1- Gamma radiation is MOST COMMON form of PE sterilization –> get oxidized PE which wears poorly and causes osteolysis***
Oxidation vs cross linking
O2 rich environment –> PE becomes oxidized –> early failure 2/2 delimitation, pitting, fatigue strength/crakcing
O2 depleted environment: PE becomes CROSS LINKED –> better resistance to adhesive and abrasive wear*
Decreased Mechanical properties –> decrease4d ductility and fatigue resistance! –> higher risk of catastrophic failure under high loads
Must package in argon or nitrogen or in vacuum*
Free radical removal:
Thermal stabilization/remelting –>? removes free radicals made during radiation sterilization for cross linking –> most effective as it occurs above PE melting point* –> changes PE from partial crystalline state to amorphous state –> this REDUCES mechanical properties*
Annealing: MAINTAINS MECHANICAL PROPERTIES –> less effective at removing free radicals! –> susceptible to oxidation ***
2 - Solution: Irraiate PE in INERT GAS (nitrogen or argon) or in vacuum to minimize oxidation***
PE manufacturing fabrication methods
Causes of failure?
Solution?
Manufacturing Methods
1-Ram bar extrusion and machining
UHMWPE powder into heated chamber, ram pushes into heated cylinder barrel –> cylindrical rod –> 10 ft length –> implants from bar stock –> get VARIATIONS in PE quality w/in bar***
2- Calcium stearate additive –> leads to fusion defects in PE
3- Sheet compression molding: UHMWPE powder into 4’ x 8’ rectangular container to make sheets up to 8” thick –> implants from molded sheets
4 - direct compression molding/net shape
UHMWPE poser into molded shape of final component –> heated –> BEST PE FABRICATION PROCESS*** –> lower wear rates but slow and expensive
Failure
Machining shear forces causes subsurface region stretching of PE chains
PE more susceptible to XRT in this region –> more oxidation –> delimitation and fatigue cracking –> Classic white band of oxidation 1-2 mm below articular surface***
Perfect storm for catastrophic wear:
Metal backed tibia w/ bone conserving tibial cut = thin PE
Flat bearing design –> low contact area with HIGH contact load
PCL retention w/ flat PE –> high sliding wear
Ram bar PE w/ calcium stearate additive –> fusion defects in PE
Gamma rad in air –> weakened mech properties of PE (oxidation)
Machine PE surface –> cutting tool stretch effect on PE
Solution
Use DIRECT COMPRESSION MOLDING of PE
Less fatigue crack formation and propagation vs ram bar extrusion*
Avoid machining of articular surface
What process changes PE from partial crystalline to amorphous state?
What process most increases wear resistance for UHMWPE?
Does annealing or remelting decrease free radicals more?
Crystalline to amorphous - Remelting***
Increases wear-resistance: Radiation –> cross linking***
Remelting reduces free radicals more***
What wear rate is ass’d with osteolysis and component loosening?
What component factor most determines wear rate for THA?
Linear wear rate > 0.1 mm/year***
Most important factor = head size***
V = 3.14r^2w (V = volumetric wear, r = head radius, w = linear head wear)
HOWEVER –> femoral head sizes between 22 and 46 do NOT influence wear rates appreciably for UHMWPE**
What factors cause greater MoM serum ion levels?
Cup abduction >55 degrees***
Smaller component sizes***
What factors do macrophages release to cause osteolysis in total joint?
Osteolytic factors/cytokines
TNA-alpha*
IL-1*
IL-6***
Increase in TNF-alpha INCREASES RANK*
increase of VEGF with UHMWPE enhances RANK and RANKL activation –> RNAKL mediated bone resorption*
How to measure bone turnover on labs?
N-telopeptide urine levels***
What size of PE particles are the most reactive?
<1 micron* –> most reactive to macrophage induced osteolysis*
What is anakinra?
What is tocilizumab?
Receptor antagonist of IL-1**
IL-1 = PRO inflammatory cytokine –> causes osteolysis***
tocilizumab = monoclonal Ab against IL-6 (another pro inflammatory cytokine that causes OSTEOLYSIS)
How much wear per year puts a prosthetic joint at risk for failure?
0.1 mm/year***
What is a normal Tonnis angle?
Measures angle of the weight bearing surface
Angle between horizontal line from medial and lateral edges of sourcil***
Normal about 10 degrees***
Lateral center edge angle?
Measures femoral head lateralization on AP pelvis
Angle formed by intersection of vertical through center of head and line extending from center of head to lateral sourcil***
Normal 25-45; <20 DIAGNOSTIC for DDH
Anterior center edge angle?
Measures ANTERIOR DYSPLASIA on FALSE PROFILE
Angle between vertical line through center of head and line going from center of head to anterior sourcil***-
normal: 25-50 degrees; <20 diagnostic for DDH
What does alpha angle check on frog leg lateral?
checking for FAI secondary to femoral head/neck offset deformity***
Anything over 42 degrees = FAI***
Cell count for infection in TKA?
Acute infection numbers?
For hips?
MoM hips?
Cell count (long standing joint) for TKA –> 1100 cells and 64% PMN***
Acute infection: 27,800 cells in first 6 weeks after TKA** (basically 30,000)
Hips: WBC >3000 and PMN >80%***
MoM hips: 4350+ cells and 85% PMN***
What does alpha anti-defensing test for?
Presence of an INTRAARTICULAR, antimicrobial peptide**
How long can an infection be considered a surgical site infection (SSI)?
one year***
What inflammatory marker has the highest correlation for PJI?
IL-6 ***
What can decrease joint reactive forces? (Acetabulum, femur, gait)
What increases forces?
Decrease joint reactive forces by shifting center of rotation medially* –> do this by:
Acetabulum: Move acetabular component medially, inferiorly and anterior*
Femur: Increase offset***
Long sem prosthesis
Lateralization of GT
Gait: shifting body weight over affected hip –> Trendelnburg gait*
Cane in contra hand* –> reduces abductor muscle pull and decreases moment arm between center of gravity and femoral head –> cane creates additional force that keeps pelvis level during unilateral stance***
Increase joint reactive forces: Valgus neck-shaft angulation –> BUT decreases shear***
How to determine joint reactive forces (equation)?
Joint reactive force = Abductor tension + 5/6(body weight) ***
Abductor tension (distance from center of rotation to greater Troch) - (5/6BW x distance from center of head to center of pubis)***
What happens in Trendelenburg gait?
The pelvis on swing side drops, causing increased adduction of the affected hip during the stance phase***
Lurch of trunk towards affected side (during stance)
Normal Q angle in extension of males? females?
Males - 13 degrees***
Females 18 degrees***
What is “screw home” mechanism of knee mechanics?
Tibia EXTERNALLY ROTATES in last 15 degrees of extension***
Due to medial tibial plateau being longer than lateral plateau***
Relevance: “locks” knee in extension to decrease work performed by quad during stance
Normal tibia-femoral joint kinematics with flexion/extension
tibia EXernally rotates on femur as the knee EXtends*** (screw home mechanism)
Tibia internally rotates during knee flexion***
Medial femoral condyle does not move much from 0-120 degrees, but lateral femoral condyle moves posteriorly***
Then both move posteriorly from 120 degrees of flexion on***
What is “paradoxical motion” used to describe knee kinematics?
Used to describe ACL deficient CR TKA***
Femur usually has “rollback” –> posterior movement of tibiofemoral contact point with knee motion from extension to flexion
In “paradoxical rollback” –> ACL deficient CR knee can’t create normal femoral rollback w/ knee flexion*** –> get ANTERIOR contact movement (happens more on medial side than lateral in kinematic trial)
Risk of femoral head collapse based on imaging - how to predict?
Based on modified Kerboul necrotic angle –> add arc of femoral head necrosis on mid-sagittal and mid-coronal MR images***
Low risk: <190 combined degrees
Moderate: 190-240
High risk: >240 degrees***
What does bone marrow edema on MRI predict in case of early AVN of hip?
Predictive of worsening pain** and future progression of dz***
Tx of femoral head AVN
Nonop?
Nonop: precollapse AVN –> can try alendronate –> shown to prevent head collapse in AVN w/ subchondral lucency***
Operative
Core decompression –> early AVN before subchondral collapse –> relieve intraosseos HTN and stimulate healing response via angiogenesis ***
Rotational osteotomy –> for small lesions (<15%) in which lesion can be rotated away from weight bearing surface –> do in IT region (varus for medial dz, valgus for anterolateral dz)
Vascularized free fibula
For young patient with either pre collapse or collapsed head –> remove necrotic area and place fibular star under subchondral bone to prevent collapse
Complications of Free fib –> sensory deficit, motor weakness, FHL contracture, tibial stress fx ***
THA
Younger patients: Higher rate of linear wear of PE and osteolysis when compared to older THA for OA***
Who does best with hip resurfacing?
Male
<55 y/o
OA patients
What % of asymptomatic patients with SCD who have AVN of femoral head will develop collapse? Pain?
75% develop collapse***
90% develop pain***
What are some of MMP’s responsible for hip OA?
What are inflammatory cytokines?
MMP’s
1 - stromelysin*
2 - plasmin **
3 - aggrecanase - 1 (ADAMTS-4)*
Inflammatory cytokines***
IL-1, IL-6, TNF-alpha
How do corticosteroid injections work?
Bind directly to nuclear receptors to interrupt the inflammatory and immune cascade via mRNA changes***
What changes are ass’d with adult hip dysplasia?
Increased femoral ante version w/ posterior GT**
Coxa valga**
Head-neck junction deformity
Femoral head asphericity
hypoplasia of femoral canal
Crowe classification of hip dysplasia
I: proximal displacement <10% vertical height of pelvis, proximal migration of head neck junction from inter-teardrop line < 50% of femoral head vertical diameter (standard THA)
II: 10-15% vertical heigh, 50-75% femoral head subluxation (uncemented cup at or near true acetabulum, may need femoral shortening)
III: 15-20% vertical displacement, 75-100% femoral head subluxation (same as II)
IV: >20% vertical displacement, >100% femoral head subluxation (Extra-small acetabular component in true acetabulum, proximal shortening or subtroch osteotomy)
Hip arthroscopy for adult DDH outcomes?
Chondral and labral pathology 2/2 osseous instability –> recurs and progresses
Ass’d with:
Accelerated progression of OA*
hip subluxation*
Increased surgical failure and reoperation***
THA for adult DDH outcomes
Outcomes for Crowe I and II initially the same as THA for OA, but long term f/u shows higher revision rates***
Increased complication profile:
Infection, instability and neuromuscular injury***
Risk of sciatic injury if limb lengthened by 4cm * (peroneal division)
Perform trochanter or subtroch osteotomy to shorten**
How much uncoverage with the super-lateral margin is acceptable in THA?
up to 30%***
Most common acute failure of hip resurfacing?
Periprosthetic femoral neck fracture***
Likely due to osteonecrosis
Risk factors:
Femoral neck notching –> by placing implant in slight varus (rather than slight valgus)***
tx: covert to THA
Risk factors for developing pseudo tumor after MoM hip resurfacing?
Female*
<40 y/o*
Small components*
Procedure done for DDH*
Why does MoM larger head not cause increased wear rates?
Larger bearings have greater sliding speed***
Higher sliding speed increases amount of fluid drawn in so get increased separation of bearing surfaces –> offsets the negative effect of increased sliding distance of the larger head***
leukocyte chromosomal aberrations are ass’d with what type of hip?
MoM hips***
What risk do lateralized liners in acetabulum carry?
Increases risk of acetabular component loosening***
What is optimal size for biologic fixation for femoral component in terms of:
Pore size?
Porosity?
Gaps?
Micromotion?
Pore size: 50- 300 micrometers (preferably 50-150 micrometers***)
Porosity 40-50% –> increased porosity leads to shearing of metal
Gaps < 50 micrometers –> gap between bone and prosthetics
Micromotion <150 micrometers –> if more get fibrous ingrowth***
Risks of acetabular screw zones:
Posterior-superior?
Posterior-inferior?
Anterior-inferior?
Anterior-superior?
Posterior-superior
“Target zone” –> ideal location for screws
Can get into sciatic if elevate hip center during revision***
Posterior-inferior
“Caution zone” –> keep screws <20 mm
At risk: Sciatic, inferior gluteal nerve and vessels, internal pudendal nerve and vessels
Anterior-inferior quadrant
“Danger zone”
At risk: Obturator nerve, vessels
Anterior-superior
“Death zone”
At risk: external iliac vessels**
Risk factors for sciatic nerve palsy after THA?
How often do post op THA sciatic palsies fully recover?
DDH*** Revision surgery*** Female*** Limb lengthening*** Post traumatic arthritis*** Surgeon self rating case as difficult***
Recovery: only 35-40% fully recover*** (Takes 12-18 months, so continue AFO during this time)
Dose of radiation and when to give for HO prophylaxis?
600-800 cGy within 24-48 hours after procedure (or 24 hours prior to procedure = just as effective)***
Co or Cr levels to get a MARS MRI?
7 ppb***
Paprosky classification of acetabular bone loss?
Type I: minimal deformity, intact rim
Type IIA: Superior bone lysis w/ intact SUPERIOR rim
Type IIB: absent superior rim, super-lateral migration
Type IIC: Localized destruction of the medial wall
Type IIIA: Bone loss from 10 am - 2 pm around rim w/ super-lateral cup migration, ISCHIAL osteolysis
Type IIIB: Bone loss from 9 am - 5 pm around rim, superomedial cup migration, Ischial osteolysis
Paprosky classification of femoral bone loss?
Type I: minimal metaphyseal bone loss
Type II: Extensive metaphyseal loss w/ intact diaphysis
Type IIIa: Extensive metadiaphyseal bone loss, min of 4 cm of intact cortical bone in diaphysis
Type IIIb: <4 cm of intact cortical bone in diaphysis
Type IV: Extensive metadiaphyseal bone loss and a non supportive diaphysis
What pathway/signaling pathway causes osteophyte formation in OA?
Indian hedgehog***
Important mediator of chondrocyte and osteoblast differentiation in endochondral bone formation***
AAOS strong evidence treatments for knee OA?
1 - NSAIDs*
2 - Tramadol*
3 - Low impact aerobic activity***
Strong against:
HA injection
Arthroscopy w/ lavage an/or debridement
Young patient with knee valgus (symptomatic), operation to perform?
Distal femoral osteotomy*** (not HTO)
Varus producing distal femoral osteotomy
Lateral femoral condyle is hypoplastic***
HTO will not correct deformity and will result in obliquity at the joint
Overall: HTO for varus knee*
Distal femoral for valgus knee*
Indications for UKA?
Contraindications?
Indications:
Older (>60), lower demand, thin (<82 kg) –> very few pts meet these criteria
Contraindications:
Inflammatory arthritis*
ACL deficiency* (absolute for mobile bearing, relative for fixed bering)
Varus (fixed) >10 degrees
Valgus (fixed) >5 degrees
Previous meniscectomy in nonop compartment
Tricompartment arthritis*
Overweight patients
Grade IV patellofemoral chondrosis/anterior knee pain*
Complications from UKA?
1 - Aseptic loosening –> most common cause of early <5 years failure ***
2- Stress fx –> always tibia
Risk factors: Penetrating posterior cortex w/ tibial guid pin, placing guidepin metal in periphery, redrilling for guid pin, undersized tibial component***
3- Intraop fx
How many degrees can be corrected for TKA on coronal plane with bony cuts alone?
20 degrees***
Any more and require extra-articular osteotomy***
What changes when PCL resected in TKA?
Increases FLEXION gap***
Females vs males with TKA?
Females have improved implant survivorship vs males***
What factors will increase Q angle in TKA?
Internally rotating femoral or tibial component*
Medializing femoral or tibial component*
Placing patellar button on lateral side (medialize this)***
What happens to handicap after TKA? THA?
Golf handicap after TKA: significantly rises***
After THA: no change***
What can cause anterior knee pain after healed HTO?
Patella baja***
Immobilization after closing wedge can precipitate anterior knee pain***
what is most common intraop fx during TKA?
Medial condyle fx***
What is starting point for retrograde nail thru TKA? what is malalignment that occurs?
Starting point is more POSTERIOR than normal***
Leads to HYPEREXTENSION***
Tx of periprosthetic fx of patella in TKA?
Nonop
Cast or brace: if stable implant with intact extensor implant
Operative
Loose patellar or extensor mech disruption***
How does lateral plating compare to retrograde nail for periprosthetic TKA fracture?
Same nonunion***
Less malunion with lateral plating (likely due to nailing having posterior start point leading to hyperextension)***
Why does TKA dislocate?
Loose flexion gap***
Popliteus cut, too much tibial slope, undersizing femoral component, anteriorizing femoral component
How to treat a partial quad tendon rupture with TKA?
Nonop***
Knee immobilizer for 6 weeks***
Risk factors for peroneal palsy after TKA?
Valgus*
Tourniquet >120 min*
Postop use of epidural
Aberrant retractor placement
Prognosis
50+% improve w/ time
What is a contraindication to using a metaphyseal sleeve?
large UNCONTAINTED defect in tibial metaphysis***
Use CONES for uncontained defects***
What approach for revision TKA with patella Baja?
Tibial tubercle osteotomy***
TKA in general population vs TKA in patient with previous tibial plateau fx?
HIGHER COMPLICATIONS***
SAME outcomes and satisfaction**
