Locking plates are a popular method of internal fixation. Locking plates are most often used as a bridging plate in fractures with bone loss and short articular fragments.
The working length of a plate includes the portion of the plate that is unsupported by bone. The longer the segment of unsupported bone, the greater is the risk of failure.
Locking plates have become a popular, effective method of stabilizing metaphyseal/epiphyseal fractures with comminution and short articular fragments.
Important biomechanical features of locking plates include1:
* Locked screws can function as individual blade plates in the distal fragment.
* Locking plates can effectively serve as bridge plates, providing excellent fixation in short distal articular fragments.
* Compression of the plate against the bone is less than that of conventional plating, resulting in less devascularization of the underlying cortex.
* There is no toggling between the locked screws and the plate.
* The pullout strength of a locked unicortical screw is approximately 60% of a standard bicortical screw.
* Locking plates are similar biomechanically to an external fixator.
* Moment arms are less because the plate is closer to the bone's neutral axis than the connecting bar of the external fixator.
This blog is dedicated to my students and orthopaedic residents who are eager to improve their orthopaedic knowledge.
Monday, July 27, 2009
Intra-articular and Soft Tissue Steroid Injections
Indications
1. Osteoarthritis and inflammatory arthritis
2. Meniscal tears
3. Tendinitis
4. Tenosynovitis
Contraindications
1. Infection
2. Allergy to steroids or lidocaine
3. Warfarin therapy
1. International normalized ratio (INR) > 4.5
Complications
1. Transient increase in pain (most common)
1. Occurs in approximately 5% of patients
2. Subsides within 24 hours
3. May be caused by the less soluble steroids
2. Skin and subcutaneous tissue atrophy
3. Depigmentation
4. Systemic effects (fairly common)
1. Usually mild and resolve quickly
2. Flushing, slight agitation
3. May worsen glucose control in patients with diabetes
5. Adrenal suppression (when given more than 1 to 2 times per month)
6. Infection occurs in 1 in 10,000 patients
Technique
1. Sterile, often helpful to anesthesize the injection area with a small needle
2. Aspirate any fluid in the joint to improve pain relief
3. Large joints: a 10-cc combination of lidocaine and steroid
4. Small joints: 1 cc to 5 cc combination of lidocaine and steroid
Efficacy
Osteoarthritis of the Knee1,2
Randomized trials have shown a significant benefit of corticosteroid injection over placebo at 1 to 3 weeks (in various studies). Using pain as an outcome measure, the benefit is not significant when studied at 6 to 12 weeks.
In one study, the presence of a joint effusion and the ability to aspirate the joint correlated with a better response to the steroid treatment.2 When comparing steroid injection to placebo, there was a significant benefit only at 1 week.
Osteoarthritis of the Hip1-2
Patients experienced a significant reduction in pain at 2 and 12 weeks; however, the effect was lost by 26 weeks.
References
1. Creamer P. Intra-articular corticosteroid treatment in osteoarthritis.Curr Opin Rheumatol.1999;11(5):417.
2. Gaffney K, Ledingham J, Perry JD. Intra-articular triamcinolone hexacetonide in knee osteoarthritis: factors influencing the clinical response.Ann Rheum Dis.1995;54:379-381.
3. Ike R. Therapeutic injection of joints and soft tissues. In:Primer on the Rheumatic Disorders.Atlanta, Ga: Arthritis Foundation; 2001.
1. Osteoarthritis and inflammatory arthritis
2. Meniscal tears
3. Tendinitis
4. Tenosynovitis
Contraindications
1. Infection
2. Allergy to steroids or lidocaine
3. Warfarin therapy
1. International normalized ratio (INR) > 4.5
Complications
1. Transient increase in pain (most common)
1. Occurs in approximately 5% of patients
2. Subsides within 24 hours
3. May be caused by the less soluble steroids
2. Skin and subcutaneous tissue atrophy
3. Depigmentation
4. Systemic effects (fairly common)
1. Usually mild and resolve quickly
2. Flushing, slight agitation
3. May worsen glucose control in patients with diabetes
5. Adrenal suppression (when given more than 1 to 2 times per month)
6. Infection occurs in 1 in 10,000 patients
Technique
1. Sterile, often helpful to anesthesize the injection area with a small needle
2. Aspirate any fluid in the joint to improve pain relief
3. Large joints: a 10-cc combination of lidocaine and steroid
4. Small joints: 1 cc to 5 cc combination of lidocaine and steroid
Efficacy
Osteoarthritis of the Knee1,2
Randomized trials have shown a significant benefit of corticosteroid injection over placebo at 1 to 3 weeks (in various studies). Using pain as an outcome measure, the benefit is not significant when studied at 6 to 12 weeks.
In one study, the presence of a joint effusion and the ability to aspirate the joint correlated with a better response to the steroid treatment.2 When comparing steroid injection to placebo, there was a significant benefit only at 1 week.
Osteoarthritis of the Hip1-2
Patients experienced a significant reduction in pain at 2 and 12 weeks; however, the effect was lost by 26 weeks.
References
1. Creamer P. Intra-articular corticosteroid treatment in osteoarthritis.Curr Opin Rheumatol.1999;11(5):417.
2. Gaffney K, Ledingham J, Perry JD. Intra-articular triamcinolone hexacetonide in knee osteoarthritis: factors influencing the clinical response.Ann Rheum Dis.1995;54:379-381.
3. Ike R. Therapeutic injection of joints and soft tissues. In:Primer on the Rheumatic Disorders.Atlanta, Ga: Arthritis Foundation; 2001.
COMPARTMENT SYNDROME
Compartment syndromes develop when the pressure in closed compartment (such as the four compartments of the leg, the anterior or posterior compartment of the thigh, or the three compartments of the forearm) rises to the point that the microvascular circulation of the muscles and nerves in the compartment are compromised.
Pathophysiology
Compartment syndromes develop when the pressure in closed compartment rises to the point that the microvascular circulation of the muscles and nerves in the compartment are compromised.
Normal compartmental pressure is 0 to 10 mmHg. When the tissue pressure rises to between 10 mm Hg and 30 mm Hg of the diastolic pressure, the perfusion of both muscle and nerve is compromised and ischemia occurs.
Important things to remember:
1. With complete ischemia, muscle remains viable for up to 3 to 4 hours without irreversible damage.
1. At 6 to 8 hours of complete ischemia, there is variable recovery.
2. More than 8 hours of complete ischemia causes irreversible muscle injury.
1. Peripheral nerves show conduction changes after 1 hour of total ischemia, the neurons and supporting structures can sustain up to 4 hours of total ischemia with a reversible injury pattern (neuropraxia - conduction defect with Wallerian degeneration).
Presentation
Patients with compartment syndrome present with severe pain that is out of proportion to their injury. The evaluation of patients is difficult and deceiving as the clinical picture can be variable. The amount of pain must be assessed carefully, and assessments should be made at multiple times, ideally by the same individual or with carefully documented progress notes. Pain is often intense, and patients with a fully evolved compartment syndrome have difficulty lying quietly - most resist the clinician palpating the leg.
The key historical finding is extreme pain. Therefore, clinicians must be extremely careful not to over medicate a patient with analgesics because medications mask the compartment syndrome.
Physical Examination
5 steps of examination:
Step 1. Visually inspect the involved limb. Does the limb appear swollen? With marked swelling, the limb will often have a circular appearance and the skin may be taut and shiny without wrinkles.
Step 2. Palpate each compartment. Is there extreme pain with palpation? Is the compartment soft or hard?
Step 3. Test motor function and grade on a scale of one to five. First ask the patient to flex and extend the digits of the involved joint. This test checks if the involved muscles move easily through the compartment. If the patient can easily flex and extend, then swelling in the compartment is probably not severe. Next, test the muscle group and grade the strength.
Step 4. Passively flex and extend the digits or joint, assessing for pain. Extreme pain on passive flexion and extension is a sign of impending compartment syndrome. The tissue pressure in the compartment has risen to the point that there is severe pain with excursion of the muscle and tendons throughout the compartment.
Step 5. Test sensory nerve function by assessing sensibility of the nerves that travel through the compartment. The ability of the patient to feel light touch should be checked first and compared from side to side. If light touch cannot be felt, then one should measure the ability of the patient to detect pin prick. One should also assess for paresthesias and dysesthesias.
Assessment and Decision-Making
After examining the patient, the clinician must decide whether the patient has: 1) no evidence of a compartment syndrome, 2) a possible or probable compartment syndrome, or a 3) definite compartment syndrome.
No evidence of a compartment syndrome
In this scenario, the patient does not have pain out of proportion to injury; the involved compartment is soft, or, if swollen, the amount of swelling is in proportion to the injury; and palpation of the compartment does not produce intense pain. Motor function is normal and any weakness noted should be within the limits one would expect for normal pain and weakness secondary to the injury.
Possible or probable compartment syndrome
In this scenario, the clinician is unsure whether the patient has elevated tissue pressure, which may indicate a compartment syndrome. The patient may have any combination of pain out of proportion to injury, a tense or painful compartment, loss of motor function or sensation, or pain on passive stretch of the muscle of the compartment. To determine whether there are elevated pressures within the compartment, the clinician must measure the pressures within the compartment. Once the compartment pressures have been measured, the clinician then compares the pressures to the diastolic pressure and makes a decision as to whether a compartment syndrome is present.
Definite compartment syndrome
A definite compartment syndrome is present when the patient has severe pain out of proportion to injury, severe pain on passive stretch of the compartment and tenseness.There may be loss of neurologic function (motor or sensory changes).
The patient should be scheduled for immediate fasciotomy of the involved limb. Compartment pressures are measured to confirm the clinician's diagnosis. The pressure measurements are performed either at the bedside or in the operating room.
Tissue Pressure Measurement
Several instruments are used to measure tissue pressure. One may use a manometer, which is an electronic device such as is available in the intensive care unit, or a custom application such as the Stryker tissue pressure measurement device.
When measuring tissue pressure in a patient with a tibial fracture, the measurement should be done at the level of the fracture.
Indications for fasciotomy
The indications for fasciotomy have varied in the literature. Some authors have recommended an absolute tissue pressure measurement, while others have advocated determining the gradient by comparing the tissue pressure to either the diastolic pressure or the mean arterial pressure. The diastolic pressure is most commonly used because one does not have to do a calculation to determine mean arterial pressure (mean arterial pressure is the diastolic pressure plus one third of the difference between the systolic and diastolic pressures).
An important point to remember is that basic science studies have shown that normal muscle perfusion remains intact with tissue pressures within 10 mm Hg of the diastolic pressure. With injured muscle, the threshold decreases to within 20 mm Hg of the diastolic pressure. With this basic science knowledge, many authors now recommend fasciotomy when the tissue pressure is within 30 mm Hg of the diastolic pressure.
References
* Heckman MM, Whitesides TE Jr, Grewe SR, Judd RL, Miller M, Lawrence JH 3rd. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993; 7:199-210.
* Heppenstall RB, Sapega AA, Scott R, Shenton D, Park YS, Maris J, Chance B. The compartment syndrome: An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop. 1988; 226:138-155.
* Heppenstall RB, Scott R, Sapega A, Park YS, Chance B. A comparative study of the tolerance of skeletal muscle to ischemia: Tourniquet application compared with acute compartment syndrome. J Bone Joint Surg Am. 1986; 68:820-828.
* Whitesides TE, Heckman MM. Acute compartment syndrome: Update on diagnosis and treatment. J Am Acad Orthop Surg. 1996; 4:209-218.
* Whitesides TE. Compartment syndromes and the role of fasciotomy, its parameters and techniques. Instr Course Lect. 1977; 26:179-196.
Pathophysiology
Compartment syndromes develop when the pressure in closed compartment rises to the point that the microvascular circulation of the muscles and nerves in the compartment are compromised.
Normal compartmental pressure is 0 to 10 mmHg. When the tissue pressure rises to between 10 mm Hg and 30 mm Hg of the diastolic pressure, the perfusion of both muscle and nerve is compromised and ischemia occurs.
Important things to remember:
1. With complete ischemia, muscle remains viable for up to 3 to 4 hours without irreversible damage.
1. At 6 to 8 hours of complete ischemia, there is variable recovery.
2. More than 8 hours of complete ischemia causes irreversible muscle injury.
1. Peripheral nerves show conduction changes after 1 hour of total ischemia, the neurons and supporting structures can sustain up to 4 hours of total ischemia with a reversible injury pattern (neuropraxia - conduction defect with Wallerian degeneration).
Presentation
Patients with compartment syndrome present with severe pain that is out of proportion to their injury. The evaluation of patients is difficult and deceiving as the clinical picture can be variable. The amount of pain must be assessed carefully, and assessments should be made at multiple times, ideally by the same individual or with carefully documented progress notes. Pain is often intense, and patients with a fully evolved compartment syndrome have difficulty lying quietly - most resist the clinician palpating the leg.
The key historical finding is extreme pain. Therefore, clinicians must be extremely careful not to over medicate a patient with analgesics because medications mask the compartment syndrome.
Physical Examination
5 steps of examination:
Step 1. Visually inspect the involved limb. Does the limb appear swollen? With marked swelling, the limb will often have a circular appearance and the skin may be taut and shiny without wrinkles.
Step 2. Palpate each compartment. Is there extreme pain with palpation? Is the compartment soft or hard?
Step 3. Test motor function and grade on a scale of one to five. First ask the patient to flex and extend the digits of the involved joint. This test checks if the involved muscles move easily through the compartment. If the patient can easily flex and extend, then swelling in the compartment is probably not severe. Next, test the muscle group and grade the strength.
Step 4. Passively flex and extend the digits or joint, assessing for pain. Extreme pain on passive flexion and extension is a sign of impending compartment syndrome. The tissue pressure in the compartment has risen to the point that there is severe pain with excursion of the muscle and tendons throughout the compartment.
Step 5. Test sensory nerve function by assessing sensibility of the nerves that travel through the compartment. The ability of the patient to feel light touch should be checked first and compared from side to side. If light touch cannot be felt, then one should measure the ability of the patient to detect pin prick. One should also assess for paresthesias and dysesthesias.
Assessment and Decision-Making
After examining the patient, the clinician must decide whether the patient has: 1) no evidence of a compartment syndrome, 2) a possible or probable compartment syndrome, or a 3) definite compartment syndrome.
No evidence of a compartment syndrome
In this scenario, the patient does not have pain out of proportion to injury; the involved compartment is soft, or, if swollen, the amount of swelling is in proportion to the injury; and palpation of the compartment does not produce intense pain. Motor function is normal and any weakness noted should be within the limits one would expect for normal pain and weakness secondary to the injury.
Possible or probable compartment syndrome
In this scenario, the clinician is unsure whether the patient has elevated tissue pressure, which may indicate a compartment syndrome. The patient may have any combination of pain out of proportion to injury, a tense or painful compartment, loss of motor function or sensation, or pain on passive stretch of the muscle of the compartment. To determine whether there are elevated pressures within the compartment, the clinician must measure the pressures within the compartment. Once the compartment pressures have been measured, the clinician then compares the pressures to the diastolic pressure and makes a decision as to whether a compartment syndrome is present.
Definite compartment syndrome
A definite compartment syndrome is present when the patient has severe pain out of proportion to injury, severe pain on passive stretch of the compartment and tenseness.There may be loss of neurologic function (motor or sensory changes).
The patient should be scheduled for immediate fasciotomy of the involved limb. Compartment pressures are measured to confirm the clinician's diagnosis. The pressure measurements are performed either at the bedside or in the operating room.
Tissue Pressure Measurement
Several instruments are used to measure tissue pressure. One may use a manometer, which is an electronic device such as is available in the intensive care unit, or a custom application such as the Stryker tissue pressure measurement device.
When measuring tissue pressure in a patient with a tibial fracture, the measurement should be done at the level of the fracture.
Indications for fasciotomy
The indications for fasciotomy have varied in the literature. Some authors have recommended an absolute tissue pressure measurement, while others have advocated determining the gradient by comparing the tissue pressure to either the diastolic pressure or the mean arterial pressure. The diastolic pressure is most commonly used because one does not have to do a calculation to determine mean arterial pressure (mean arterial pressure is the diastolic pressure plus one third of the difference between the systolic and diastolic pressures).
An important point to remember is that basic science studies have shown that normal muscle perfusion remains intact with tissue pressures within 10 mm Hg of the diastolic pressure. With injured muscle, the threshold decreases to within 20 mm Hg of the diastolic pressure. With this basic science knowledge, many authors now recommend fasciotomy when the tissue pressure is within 30 mm Hg of the diastolic pressure.
References
* Heckman MM, Whitesides TE Jr, Grewe SR, Judd RL, Miller M, Lawrence JH 3rd. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993; 7:199-210.
* Heppenstall RB, Sapega AA, Scott R, Shenton D, Park YS, Maris J, Chance B. The compartment syndrome: An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop. 1988; 226:138-155.
* Heppenstall RB, Scott R, Sapega A, Park YS, Chance B. A comparative study of the tolerance of skeletal muscle to ischemia: Tourniquet application compared with acute compartment syndrome. J Bone Joint Surg Am. 1986; 68:820-828.
* Whitesides TE, Heckman MM. Acute compartment syndrome: Update on diagnosis and treatment. J Am Acad Orthop Surg. 1996; 4:209-218.
* Whitesides TE. Compartment syndromes and the role of fasciotomy, its parameters and techniques. Instr Course Lect. 1977; 26:179-196.
Articular Cartilage
Frank J. Frassica, MD
Important properties of articular cartilage include:
* Avascular (no blood vessels)
* Aneural (no nerve fibers)
* Alymphatic (no lymphatic vessels)
* Very low friction on cartilage on cartilage motion
* Self-renewing (maintenance and restoration of extracellular matrix)
* With aging, loss of ability to maintain the extracellular matrix
In regard to chondrocytes:
* By cartilage volume, the cells only represent about 1%.
* Chondrocytes are synthetic machines producing the extracellular matrix.
o Intracellular organelles
+ Endoplasmic reticulum
+ Golgi apparatus
* Chondrocytes do not have cell-to-cell contact in the extracellular matrix.
* With aging, chondrocytes lose their synthetic abilities.
* Chondrocytes respond to a number of stimuli:
o Increase matrix production after sensing degradation of the matrix
o Sense loads and increase matrix production
o Respond to growth factors and anabolic stimuli
Articular cartilage has three principal classes of macromolecules:
* Collagen – 60%
* Proteoglycans – 25% to 35%
* Noncollagenous proteins/glycoproteins – 15% to 20%
The three articular cartilage collagens that form cross bands are types II, IX, and XI.
Of particular note:
* Type XI binds to type II.
* Type IX binds to the cross-banded fibrils in the superficial layer.
* Type VI attaches to the matrix around the chondrocytes.
* Type X is near the calcified layer and is probably involved in mineralization of the calcified layer.
Noncollagenous proteins include:
* Decorin and fibromodulin bind to type II collagen and likely stabilize the type II collagen network.
Cartilage has a number of distinct zones.
The superficial zone has a number of important characteristics:
* Thinnest articular cartilage layer
* Two layers:
o Most superficial – fine collagen fibrils (lamina splendens)
o Deep layer – flattened fibroblast-like chondrocytes (parallel to joint surface)
* Forms a cartilage skin
* Important chemical properties:
o High collagen and low proteoglycan concentration
o Fibronectin and water concentrations are highest in this zone
* Great tensile stiffness and strength
* Seals off the cartilage from the immune system
The transitional zone lies between the superficial and middle zones of the articular cartilage.
The following important points should be remembered:
* The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
* The collagen fibers are larger than in the superficial zone.
* The proteoglycan concentration is higher than the superficial zone.
The chondrocytes in the calcified cartilage zone show the least metabolic activity.
In contrast, the chondrocytes of the other areas are very active:
* Superficial zone
o Fine collagen fibrils (lamina splendens)
o High collagen and low proteoglycan concentration
o Fibronectin and water concentrations are highest in this zone
* Transitional zone
o The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
o The collagen fibers are larger than in the superficial zone.
o The proteoglycan concentration is higher than the superficial zone.
* Middle (radial or deep) zone
o Largest diameter collagen fibrils
o Highest proteoglycan content
Other important points:
Interleukin I has the potential to increase expression of matrix metalloproteinases that can dissolve the extracellular matrix.
Type II collagen fibers resist tensile and shear deformation forces in the articular cartilage.
In contrast, the glycosaminoglycan aggregates resist articular cartilage compression and fluid flow.
Cyclic compressive loads have the ability to stimulate matrix synthesis – aggrecan core protein and the glycosaminoglycans.
The characteristic findings in osteoarthritis are:
* Asymmetric loss of the joint space
* Subchondral sclerosis and cysts
* Osteophyte formation
Osteoarthritis
As the cartilage degenerates, progressive bone remodeling occurs. The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
* Constant type II collagen content
* Decreased proteoglycan concentration and decreased chain length
* Increased water content
The decreased proteoglycan content results in increased permeability of the cartilage. A reduction of the stiffness makes the articular cartilage less able to bear loads.
In the second stage, there is a cellular response – chondrocyte proliferation. Clusters of chondrocytes producing new matrix are visible.
In this stage, there is nitric oxide and interleukin I production. These are catabolic factors that increase matrix metalloproteinase activity. Degradative enzymes break down types IX and XI collagen, which may compromise the stability of the type II collagen framework.
In the last stage of osteoarthritis, there is reduced chondrocyte proliferation and function, which may be secondary to reduced ability to respond to anabolic factors (down regulation). There may be accumulation of molecules that bind to the anabolic factors (and keep the factors from the chondrocytes) such as decorin and insulin-dependent growth factor binding protein.
Bibliography
1. Mankin HJ, Grodzinsky AJ, Buckwalter JA. Articular cartilage and osteoarthritis. In: Einhorn TA, O’Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science. 3rd ed. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 2007:161-174.
Important properties of articular cartilage include:
* Avascular (no blood vessels)
* Aneural (no nerve fibers)
* Alymphatic (no lymphatic vessels)
* Very low friction on cartilage on cartilage motion
* Self-renewing (maintenance and restoration of extracellular matrix)
* With aging, loss of ability to maintain the extracellular matrix
In regard to chondrocytes:
* By cartilage volume, the cells only represent about 1%.
* Chondrocytes are synthetic machines producing the extracellular matrix.
o Intracellular organelles
+ Endoplasmic reticulum
+ Golgi apparatus
* Chondrocytes do not have cell-to-cell contact in the extracellular matrix.
* With aging, chondrocytes lose their synthetic abilities.
* Chondrocytes respond to a number of stimuli:
o Increase matrix production after sensing degradation of the matrix
o Sense loads and increase matrix production
o Respond to growth factors and anabolic stimuli
Articular cartilage has three principal classes of macromolecules:
* Collagen – 60%
* Proteoglycans – 25% to 35%
* Noncollagenous proteins/glycoproteins – 15% to 20%
The three articular cartilage collagens that form cross bands are types II, IX, and XI.
Of particular note:
* Type XI binds to type II.
* Type IX binds to the cross-banded fibrils in the superficial layer.
* Type VI attaches to the matrix around the chondrocytes.
* Type X is near the calcified layer and is probably involved in mineralization of the calcified layer.
Noncollagenous proteins include:
* Decorin and fibromodulin bind to type II collagen and likely stabilize the type II collagen network.
Cartilage has a number of distinct zones.
The superficial zone has a number of important characteristics:
* Thinnest articular cartilage layer
* Two layers:
o Most superficial – fine collagen fibrils (lamina splendens)
o Deep layer – flattened fibroblast-like chondrocytes (parallel to joint surface)
* Forms a cartilage skin
* Important chemical properties:
o High collagen and low proteoglycan concentration
o Fibronectin and water concentrations are highest in this zone
* Great tensile stiffness and strength
* Seals off the cartilage from the immune system
The transitional zone lies between the superficial and middle zones of the articular cartilage.
The following important points should be remembered:
* The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
* The collagen fibers are larger than in the superficial zone.
* The proteoglycan concentration is higher than the superficial zone.
The chondrocytes in the calcified cartilage zone show the least metabolic activity.
In contrast, the chondrocytes of the other areas are very active:
* Superficial zone
o Fine collagen fibrils (lamina splendens)
o High collagen and low proteoglycan concentration
o Fibronectin and water concentrations are highest in this zone
* Transitional zone
o The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
o The collagen fibers are larger than in the superficial zone.
o The proteoglycan concentration is higher than the superficial zone.
* Middle (radial or deep) zone
o Largest diameter collagen fibrils
o Highest proteoglycan content
Other important points:
Interleukin I has the potential to increase expression of matrix metalloproteinases that can dissolve the extracellular matrix.
Type II collagen fibers resist tensile and shear deformation forces in the articular cartilage.
In contrast, the glycosaminoglycan aggregates resist articular cartilage compression and fluid flow.
Cyclic compressive loads have the ability to stimulate matrix synthesis – aggrecan core protein and the glycosaminoglycans.
The characteristic findings in osteoarthritis are:
* Asymmetric loss of the joint space
* Subchondral sclerosis and cysts
* Osteophyte formation
Osteoarthritis
As the cartilage degenerates, progressive bone remodeling occurs. The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
* Constant type II collagen content
* Decreased proteoglycan concentration and decreased chain length
* Increased water content
The decreased proteoglycan content results in increased permeability of the cartilage. A reduction of the stiffness makes the articular cartilage less able to bear loads.
In the second stage, there is a cellular response – chondrocyte proliferation. Clusters of chondrocytes producing new matrix are visible.
In this stage, there is nitric oxide and interleukin I production. These are catabolic factors that increase matrix metalloproteinase activity. Degradative enzymes break down types IX and XI collagen, which may compromise the stability of the type II collagen framework.
In the last stage of osteoarthritis, there is reduced chondrocyte proliferation and function, which may be secondary to reduced ability to respond to anabolic factors (down regulation). There may be accumulation of molecules that bind to the anabolic factors (and keep the factors from the chondrocytes) such as decorin and insulin-dependent growth factor binding protein.
Bibliography
1. Mankin HJ, Grodzinsky AJ, Buckwalter JA. Articular cartilage and osteoarthritis. In: Einhorn TA, O’Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science. 3rd ed. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 2007:161-174.
Total Knee Replacement: Technique Basics
Templating for Total Knee Replacement
The physical examination should include an analysis of alignment, ligamentous stability, range of motion and muscle strength and function.
These factors, coupled with a radiographic analysis, form the basis for preoperative planning.
Preoperative analysis radiographic analysis: standing anterior-posterior (AP) view, lateral view, and patellar-femoral view.
Survivorship of TKA is directly related to appropriate alignment and balance.
Surgeons should evaluate the biomechanics of knee alignment and determine the proper position of the implant on the mechanical axis. A long-standing radiograph should be obtained.
The process of establishing a femoral cut.
The distal femoral cut is not only important for maintaining varus and valgus positioning but also for maintaining the level of the joint line.
This is particularly challenging for the valgus knee in which the lateral femoral condyle is distally and posteriorly hyperplastic.
Intramedullary and extramedullary alignment guides can be used to accurately bring the distal femoral cut perpendicular to the mechanical axis in the AP plane.
Posterior condyles affect femoral rotation, especially in the valgus knee.
There are advantages of externally rotating the femoral component to approximately the epicondylar axis.
Varus Knee Management Techniques
Because varus deformity is the most common deformity in osteoarthritic knees, familiarity with medial or varus release techniques is a must for orthopedic surgeons performing TKA.
With a standard median patella approach, the first portion of a medial release is performed when the deep portion of the medial collateral ligament is released.
Some surgeons favours a subperiosteal release that does not include the pes anserinus (PES) insertion.
This release is carried posteriorly to include the semimembranous insertion on varus knees but not valgus knees.
The second portion of the release is removal of osteophytes that tent the medial collateral ligament.
With severe deformities, the posterior medial capsule must be released subperiosteally from the tibia to allow correction of the deformity.
The true medial release is performed for further correction, subperiosteally, distal to the PES insertion (but deep to the PES insertion) until the desired correction is obtained.
If medial release for a varus deformity is done in a step-wise and graded fashion, it can titrate the correction needed and allow normal ligamentous balance.
Valgus Knee Management Techniques
The valgus deformity is more complex and difficult than that done in varus knees.
Most surgeons prefer the median parapatellar incision over the median incision because this technique is easy. First, place the alignment jigs for bony cuts. Once the cuts are done, balance the soft tissues. Release the iliotibial band off Gerdy's tubercle while the lateral capsule is released from the tibia to the posterior lateral corner.
High valgus deformities require a lateral collateral ligament and popliteus, in that order, to be released from the epicondyle on the femur.
More release can be obtained by taking down the intramuscular septum and lateral gastrocnemius.
The posterior cruciate ligament plays a role in maintaining high valgus deformities.
Thus, resection of this ligament is usually required.
A lax medial collateral ligament may also contribute to this type of deformity.
References
1. Morawa MD. Templating for total knee replacement. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12- 16, 2000.
2. Reilly DT. Varus knee management techniques. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
3. Wright RJ. Valgus knee management techniques. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
The physical examination should include an analysis of alignment, ligamentous stability, range of motion and muscle strength and function.
These factors, coupled with a radiographic analysis, form the basis for preoperative planning.
Preoperative analysis radiographic analysis: standing anterior-posterior (AP) view, lateral view, and patellar-femoral view.
Survivorship of TKA is directly related to appropriate alignment and balance.
Surgeons should evaluate the biomechanics of knee alignment and determine the proper position of the implant on the mechanical axis. A long-standing radiograph should be obtained.
The process of establishing a femoral cut.
The distal femoral cut is not only important for maintaining varus and valgus positioning but also for maintaining the level of the joint line.
This is particularly challenging for the valgus knee in which the lateral femoral condyle is distally and posteriorly hyperplastic.
Intramedullary and extramedullary alignment guides can be used to accurately bring the distal femoral cut perpendicular to the mechanical axis in the AP plane.
Posterior condyles affect femoral rotation, especially in the valgus knee.
There are advantages of externally rotating the femoral component to approximately the epicondylar axis.
Varus Knee Management Techniques
Because varus deformity is the most common deformity in osteoarthritic knees, familiarity with medial or varus release techniques is a must for orthopedic surgeons performing TKA.
With a standard median patella approach, the first portion of a medial release is performed when the deep portion of the medial collateral ligament is released.
Some surgeons favours a subperiosteal release that does not include the pes anserinus (PES) insertion.
This release is carried posteriorly to include the semimembranous insertion on varus knees but not valgus knees.
The second portion of the release is removal of osteophytes that tent the medial collateral ligament.
With severe deformities, the posterior medial capsule must be released subperiosteally from the tibia to allow correction of the deformity.
The true medial release is performed for further correction, subperiosteally, distal to the PES insertion (but deep to the PES insertion) until the desired correction is obtained.
If medial release for a varus deformity is done in a step-wise and graded fashion, it can titrate the correction needed and allow normal ligamentous balance.
Valgus Knee Management Techniques
The valgus deformity is more complex and difficult than that done in varus knees.
Most surgeons prefer the median parapatellar incision over the median incision because this technique is easy. First, place the alignment jigs for bony cuts. Once the cuts are done, balance the soft tissues. Release the iliotibial band off Gerdy's tubercle while the lateral capsule is released from the tibia to the posterior lateral corner.
High valgus deformities require a lateral collateral ligament and popliteus, in that order, to be released from the epicondyle on the femur.
More release can be obtained by taking down the intramuscular septum and lateral gastrocnemius.
The posterior cruciate ligament plays a role in maintaining high valgus deformities.
Thus, resection of this ligament is usually required.
A lax medial collateral ligament may also contribute to this type of deformity.
References
1. Morawa MD. Templating for total knee replacement. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12- 16, 2000.
2. Reilly DT. Varus knee management techniques. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
3. Wright RJ. Valgus knee management techniques. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
Issues in Revision Total Knee Replacement
Donald T. Reilly, MD. PhD
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Donald T. Reilly, MD, PhD, moderated a group of presentations on issues in revision total knee arthroplasty (TKA).
Identifying Bony Landmarks in Revision Total Knee Replacement
Revision total knee replacement poses problems for the orthopedic surgeon because the loosening process destroys many anatomical landmarks. The first mutation to ascertain is that of full extension. Kenneth A. Krackow, MD, described a modification of his positioning jigs with a perpendicular marker from the femoral component with which to define full extension.
Soft tissue cannot be used as a guide for rotational alignment of the femoral component in revision surgery because the loosening process changes tissue tension, especially in the flexion space. External rotation of the femoral component closes the lateral flexion space and moves the asymmetry that is created by a perpendicular tibial cut. This femoral rotation can cause a varus or valgus malalignment in flexion. Krackow suggested using the epicondylar axis as the bony landmark to avoid excessive external rotation of the femoral component. The epicondylar axis should be ascertained independent of the bony condyles because these change dramatically in the revision setting. Soft tissue release for alignment in extension causes external rotation of the bony femur. As such, posterior bony cuts must not follow component positioning via this technique.
Tibial component rotation takes into account the (medial-lateral) M-L axis, A-P axis, and tibial tubercle. The foot is a poor landmark for tibial rotation because common deformities can significantly change its alignment. Instead, the tibial component should be matched in rotation to the femoral component in extension, with the soft tissue being used as a secondary guide for tibial orientation.
Soft Tissue Balancing on Revision Total Knee Replacement
Chitranjan S. Ranawat, MD, proposed that revision soft tissue balancing is similar to primary knee balancing. He described his method of creating medial lateral subperiosteal sleeves for exposing a stiff knee. This method releases essentially all soft tissue medially and laterally from the femur, allowing exposure of the distal femur for implantation. If there is a discrepancy in the soft tissue balancing between flexion and extension, then a constrained component is used with this exposure.
A tibial ion rod is used for the tibial cut, and axial rotation of the tibial component is deferred until the femoral component position is fixed. In revision surgery, tibial components that are smaller than the femoral component are often required. For the femoral side, Ranawat urges preservation of distal femoral bone. The joint line should be approximately 25 mm distal to the medial collateral attachment. The tibial insert should be of sufficient thickness to place tension on the soft tissue sleeve.
For valgus knees, Ranawat suggests lengthening the iliotibial band by using a "pie crust" technique with multiple stab incisions until a balanced knee is achieved. Releases should be done to allow a springiness of 2 to 4 mm in extension and 2 to 4 mm in flexion, both medially and laterally with distraction. Flexion instability is compensated for by a TC-3-type component. Ranawat emphasized the importance of wide exposure, preservation of bone with extraction, and use of modularity.
Revision of the Patellofemoral Joint
Although the patellar-femoral joint accounts for only 1% to 12% of complications in most TKA series, it causes of 40% to 50% of revisions in those series. James A. D'Antonio, MD, discussed revision resulting from patellofemoral joint problems, including fracture, loosening, pain, and instability of the patella.
D'Antonio and colleagues evaluated a series of 161 TKAs with resurfaced patella. At 5-year follow-up, the complication rate in the patellar-femoral joint was 5%. Improvement of patella complications is dependent on the cause. Prosthetic component placement, soft tissue problems, malposition of the femoral component, and design (especially metal back patellar components) are the most common causes of patella complications.
At least 5 to 6 mm of bone stock are required for surfacing in the revision setting. If less than 5 mm are available, patelloplasty must be done, according to D'Antonio. He believes that extensor malalignment should be addressed distally so that smaller bony changes can be performed. Treatment of patella fracture depends on the integrity of the extensor mechanism and whether the prosthetic patella is loose.
The series by Berry and Rand was presented, showing that patellar-femoral complications were the reason for 33% of revisions and that the revisions were subsequently associated with a relatively high complication rate. Patella-backed components should not be used.
Allograft for Bone Loss
Bone defects in the tibial plateau present technical problems in primary knee replacement surgery. However, variety of techniques are available to solve these problems. Lester S. Borden, MD, finds classification systems for bony defects such as that described by Rand[4] to be cumbersome and to lack utility in the revision setting. Borden proposed 20 mm as the size from which the differential between graft and augmentations should be decided. He stressed the importance of retaining as much cortical rim as possible and emphasized that surgeons performing revision should start with conservative bone cuts. Cancellous allograft impaction techniques can be used with cavitary defects and the component should have maximum coverage without overhang. Cancellous morsalized grafts should be avoided in segmental defects.
Whiteside[5] used morsalized cancellous allograft to fill large femoral and/or tibial defects in 63 patients (63 knees) who had revision surgery for failed arthroplasty between September 1988 and January 1993. Fourteen of the 63 revisions required yet another procedure between 3 weeks and 37 months after the revision surgery for loosening, wound avulsion, wound hematoma, painful wires, patellar tendon avulsion from the tibial tubercle, patellar subluxation, or late-onset instability.
Cement can be used for small defects that are less than 20 mm in depth and account for less than 50% of the surface area of revised tibia.[5] Lotke and colleagues[6] followed 59 patients treated with a cement fill for an average of 7.1 years. Only 1 of the fills failed, but 43 had radiolucent lines. Radiolucent lines were not correlated with clinical symptoms.
Windsor and colleagues[7] found that autograft in primary knees healed well in a series of 50 knees with defects. Wedges or blocks used for tibial defects showed the same pattern of strain[8]. The shape of the augmentation should be based on the shape of the defect.
Borden noted that although femoral bone loss is rare in primary TKA, it occurs in 25% of revisions. Grafting or augmentation to fill these defects is important to maintain the joint line. In young patients with large defects, a "tumor" type of approach should be avoided and bulk allografts should be used for stock augmentation. In summary, cavitary lesions should have cancellous grafting, and modularity has replaced the need for most bone grafts in segmental defects smaller than 20 mm.
Cases You Would Rather Refer
Joseph C. McCarthy, MD,[9] discussed particularly challenging cases in revision TKA. Poor outcomes in TKA are associated with:
• previous trauma
• previous surgery
• extensor mechanism failure
• osteoporosis
• compromised skin
• severe deformity
• neuropathic joints
• drug dependence
• morbid obesity.
McCarthy discussed postoperative reflex sympathetic dystrophy and stressed that inclusion of a pain service in treatment is very important. Loss of the extensor mechanism can be treated with allograft augmentation[10]; however, this procedure is associated with many complications, including extensor weakness and poor range of motion.
McCarthy discussed the role of Workers' Compensation in TKA. Mont and colleagues studied the influence of Workers' Compensation on the outcome of TKA in 42 patients who had been managed between January 1980 and December 1993. These patients were matched with a group of 32 patients who were not receiving compensation. After a mean time of 80 months, patients receiving compensation had a mean Knee Society score of 64 points. The patients who were not receiving compensation had a mean Knee Society score of 93 points. The difference between the two groups with regard to fair or poor results and revisions was significant (P <.01). Surgeons should be aware that Workers' Compensation is one of several variables that may have an untoward influence on the perceived outcome of total knee arthroplasty.
References
1. Krackow KA. Identifying bony landmarks in revision total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
2. Ranawat CS. Soft tissue balancing on revision total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
3. Antonio JA. Revision of the patellofemoral joint . State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
4. Rand JA. Bone deficiency in total knee arthroplasty. Use of metal wedge augmentation. 1991;271:63-71.
5. Whiteside LA, Bicalho PS. Radiologic and histologic analysis of morselized allograft in revision total knee replacement. Clin Orthop. 1998;357:149-156.
6. Lotke PA, Wong RY, Ecker ML The use of methylmethacrylate in primary total knee replacements with large tibial defects. Clin Orthop. 1991;270:288-294.
7. Windsor RE, Insall JN, Sculco TP Bone grafting of tibial defects in primary and revision total knee arthroplasty. Clin Orthop. 1986;205:132-137.
8. Fehring TK, Peindl RD, Humble RS, Harrow ME, Frick SL. Modular tibial augmentations in total knee arthroplasty. Clin Orthop. 1996;327:207-217.
9. McCarthy JC. Cases you would rather refer away. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
10. Emerson RH Jr, Head WC, Malinin TI. Extensor mechanism reconstruction with an allograft after total knee arthroplasty. Clin Orthop. 1994;303:79-85.
11. Mont MA, Mayerson JA, Krackow KA, Hungerford DS. Total knee arthroplasty in patients receiving Workers' Compensation. J Bone Joint Surg Am. 1998;80:1285-1290.
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Donald T. Reilly, MD, PhD, moderated a group of presentations on issues in revision total knee arthroplasty (TKA).
Identifying Bony Landmarks in Revision Total Knee Replacement
Revision total knee replacement poses problems for the orthopedic surgeon because the loosening process destroys many anatomical landmarks. The first mutation to ascertain is that of full extension. Kenneth A. Krackow, MD, described a modification of his positioning jigs with a perpendicular marker from the femoral component with which to define full extension.
Soft tissue cannot be used as a guide for rotational alignment of the femoral component in revision surgery because the loosening process changes tissue tension, especially in the flexion space. External rotation of the femoral component closes the lateral flexion space and moves the asymmetry that is created by a perpendicular tibial cut. This femoral rotation can cause a varus or valgus malalignment in flexion. Krackow suggested using the epicondylar axis as the bony landmark to avoid excessive external rotation of the femoral component. The epicondylar axis should be ascertained independent of the bony condyles because these change dramatically in the revision setting. Soft tissue release for alignment in extension causes external rotation of the bony femur. As such, posterior bony cuts must not follow component positioning via this technique.
Tibial component rotation takes into account the (medial-lateral) M-L axis, A-P axis, and tibial tubercle. The foot is a poor landmark for tibial rotation because common deformities can significantly change its alignment. Instead, the tibial component should be matched in rotation to the femoral component in extension, with the soft tissue being used as a secondary guide for tibial orientation.
Soft Tissue Balancing on Revision Total Knee Replacement
Chitranjan S. Ranawat, MD, proposed that revision soft tissue balancing is similar to primary knee balancing. He described his method of creating medial lateral subperiosteal sleeves for exposing a stiff knee. This method releases essentially all soft tissue medially and laterally from the femur, allowing exposure of the distal femur for implantation. If there is a discrepancy in the soft tissue balancing between flexion and extension, then a constrained component is used with this exposure.
A tibial ion rod is used for the tibial cut, and axial rotation of the tibial component is deferred until the femoral component position is fixed. In revision surgery, tibial components that are smaller than the femoral component are often required. For the femoral side, Ranawat urges preservation of distal femoral bone. The joint line should be approximately 25 mm distal to the medial collateral attachment. The tibial insert should be of sufficient thickness to place tension on the soft tissue sleeve.
For valgus knees, Ranawat suggests lengthening the iliotibial band by using a "pie crust" technique with multiple stab incisions until a balanced knee is achieved. Releases should be done to allow a springiness of 2 to 4 mm in extension and 2 to 4 mm in flexion, both medially and laterally with distraction. Flexion instability is compensated for by a TC-3-type component. Ranawat emphasized the importance of wide exposure, preservation of bone with extraction, and use of modularity.
Revision of the Patellofemoral Joint
Although the patellar-femoral joint accounts for only 1% to 12% of complications in most TKA series, it causes of 40% to 50% of revisions in those series. James A. D'Antonio, MD, discussed revision resulting from patellofemoral joint problems, including fracture, loosening, pain, and instability of the patella.
D'Antonio and colleagues evaluated a series of 161 TKAs with resurfaced patella. At 5-year follow-up, the complication rate in the patellar-femoral joint was 5%. Improvement of patella complications is dependent on the cause. Prosthetic component placement, soft tissue problems, malposition of the femoral component, and design (especially metal back patellar components) are the most common causes of patella complications.
At least 5 to 6 mm of bone stock are required for surfacing in the revision setting. If less than 5 mm are available, patelloplasty must be done, according to D'Antonio. He believes that extensor malalignment should be addressed distally so that smaller bony changes can be performed. Treatment of patella fracture depends on the integrity of the extensor mechanism and whether the prosthetic patella is loose.
The series by Berry and Rand was presented, showing that patellar-femoral complications were the reason for 33% of revisions and that the revisions were subsequently associated with a relatively high complication rate. Patella-backed components should not be used.
Allograft for Bone Loss
Bone defects in the tibial plateau present technical problems in primary knee replacement surgery. However, variety of techniques are available to solve these problems. Lester S. Borden, MD, finds classification systems for bony defects such as that described by Rand[4] to be cumbersome and to lack utility in the revision setting. Borden proposed 20 mm as the size from which the differential between graft and augmentations should be decided. He stressed the importance of retaining as much cortical rim as possible and emphasized that surgeons performing revision should start with conservative bone cuts. Cancellous allograft impaction techniques can be used with cavitary defects and the component should have maximum coverage without overhang. Cancellous morsalized grafts should be avoided in segmental defects.
Whiteside[5] used morsalized cancellous allograft to fill large femoral and/or tibial defects in 63 patients (63 knees) who had revision surgery for failed arthroplasty between September 1988 and January 1993. Fourteen of the 63 revisions required yet another procedure between 3 weeks and 37 months after the revision surgery for loosening, wound avulsion, wound hematoma, painful wires, patellar tendon avulsion from the tibial tubercle, patellar subluxation, or late-onset instability.
Cement can be used for small defects that are less than 20 mm in depth and account for less than 50% of the surface area of revised tibia.[5] Lotke and colleagues[6] followed 59 patients treated with a cement fill for an average of 7.1 years. Only 1 of the fills failed, but 43 had radiolucent lines. Radiolucent lines were not correlated with clinical symptoms.
Windsor and colleagues[7] found that autograft in primary knees healed well in a series of 50 knees with defects. Wedges or blocks used for tibial defects showed the same pattern of strain[8]. The shape of the augmentation should be based on the shape of the defect.
Borden noted that although femoral bone loss is rare in primary TKA, it occurs in 25% of revisions. Grafting or augmentation to fill these defects is important to maintain the joint line. In young patients with large defects, a "tumor" type of approach should be avoided and bulk allografts should be used for stock augmentation. In summary, cavitary lesions should have cancellous grafting, and modularity has replaced the need for most bone grafts in segmental defects smaller than 20 mm.
Cases You Would Rather Refer
Joseph C. McCarthy, MD,[9] discussed particularly challenging cases in revision TKA. Poor outcomes in TKA are associated with:
• previous trauma
• previous surgery
• extensor mechanism failure
• osteoporosis
• compromised skin
• severe deformity
• neuropathic joints
• drug dependence
• morbid obesity.
McCarthy discussed postoperative reflex sympathetic dystrophy and stressed that inclusion of a pain service in treatment is very important. Loss of the extensor mechanism can be treated with allograft augmentation[10]; however, this procedure is associated with many complications, including extensor weakness and poor range of motion.
McCarthy discussed the role of Workers' Compensation in TKA. Mont and colleagues studied the influence of Workers' Compensation on the outcome of TKA in 42 patients who had been managed between January 1980 and December 1993. These patients were matched with a group of 32 patients who were not receiving compensation. After a mean time of 80 months, patients receiving compensation had a mean Knee Society score of 64 points. The patients who were not receiving compensation had a mean Knee Society score of 93 points. The difference between the two groups with regard to fair or poor results and revisions was significant (P <.01). Surgeons should be aware that Workers' Compensation is one of several variables that may have an untoward influence on the perceived outcome of total knee arthroplasty.
References
1. Krackow KA. Identifying bony landmarks in revision total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
2. Ranawat CS. Soft tissue balancing on revision total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
3. Antonio JA. Revision of the patellofemoral joint . State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
4. Rand JA. Bone deficiency in total knee arthroplasty. Use of metal wedge augmentation. 1991;271:63-71.
5. Whiteside LA, Bicalho PS. Radiologic and histologic analysis of morselized allograft in revision total knee replacement. Clin Orthop. 1998;357:149-156.
6. Lotke PA, Wong RY, Ecker ML The use of methylmethacrylate in primary total knee replacements with large tibial defects. Clin Orthop. 1991;270:288-294.
7. Windsor RE, Insall JN, Sculco TP Bone grafting of tibial defects in primary and revision total knee arthroplasty. Clin Orthop. 1986;205:132-137.
8. Fehring TK, Peindl RD, Humble RS, Harrow ME, Frick SL. Modular tibial augmentations in total knee arthroplasty. Clin Orthop. 1996;327:207-217.
9. McCarthy JC. Cases you would rather refer away. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
10. Emerson RH Jr, Head WC, Malinin TI. Extensor mechanism reconstruction with an allograft after total knee arthroplasty. Clin Orthop. 1994;303:79-85.
11. Mont MA, Mayerson JA, Krackow KA, Hungerford DS. Total knee arthroplasty in patients receiving Workers' Compensation. J Bone Joint Surg Am. 1998;80:1285-1290.
Primary Total Knee Replacement: Results
Donald T. Reilly, MD. PhD
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, James A. D'Antonio, MD, moderated a group of presentations on results of various designs in total knee arthroplasty (TKA).
Results of Porous Coated Total Knee Replacement
Lester S. Borden, MD,[1] acknowledged that cemented TKA is the "gold standard." Early designs of uncemented components were developed in an attempt to eliminate the need for cement and to prevent "cement disease." Surgeons wanted more stable bony ingrowth. Eventually "cement disease" was recognized as particle disease (mostly from polyethylene wear into crevices).
The original and most successful TKA, the porous coated anatomical (PCA) artificial total knee joints, were introduced in the early 1980s. These joints were designed for bony ingrowth and to provide for normal knee kinematics. The design also introduced modularity of the tibial components. To allow for more normal kinematics, the lack of constraint dictated a "flat-on-flat" design. This resulted in a very high rate of polyethylene wear and a revision rate of 10% per year. This design, however, contributed to the development of instrumentation for alignment of components.
Thin polyethylene, when subjected to high stresses, tends to wear excessively. This has been a major contributing factor to wear in all designs. Bartel and colleagues[2] examined polyethylene stresses in patellar components with convex-shaped articulating surfaces that contacted convex metallic surfaces. For patellar models, the von Mises stress was at or near the polyethylene yield stress in most of the contact area, which is consistent with the permanent deformation observed in many retrieved components. As such, deformation may continue, even when the component's surface has deformed and been worn into a concave shape.
Fehring and colleagues[3] evaluated 20 patients referred for pain and disability after TKA with fluoroscopy-guided radiographs. Fourteen of the 20 patients had radiolucent lines in their prostheses during this evaluation. All loose components as determined by fluoroscopy were confirmed on revision.
Fluoroscopy-guided radiographs can be helpful in evaluating the patient with a painful TKA and normal-appearing office radiographs. Newer uncemented total knee designs have improved anatomical shapes and contact areas and use screws for additional fixation. These enhancements have led to improved results with uncemented knee designs.
Results with an Hydroxyapatite-Coated Total Knee Design
Jean-Alain Epinette, MD,[4] opened by reviewing the prospective randomized analysis of Nilsson and colleagues[5] in which fixation of hydroxyapatite (HA)-coated designs in 29 knees were compared with cemented tibial components in 28 knees in the Tricon II TKA. Radiostereometric analysis revealed continuous migration of cemented components compared with slight unprogressive migration of HA-coated components. In the 40 patients (19 HA-coated, 21 cemented) remaining after 5 years, the HA-coated implants had most of their migration occurring within the initial 3 months but then stabilized, whereas the cemented implants showed an initially lower -- but over time continuously increasing -- migration.
Epinette's experience with 309 knees follow after a mean of 5 years (range 0 to 9 years) showed no mechanical failure in the femoral or tibial component. Eight of these knees required a repeated procedure for patella problems. Epinette found that HA filled in radiolucent gaps in follow-up radiographs.
Results With an All-Polyethylene Tibial Component
Evolution in TKA tibial component design has centered around metal tibial trays with improved stress transfer to the proximal tibia[6] and better fixation with pegs and cement. Benefits of metal tibial trays include durable fixation and modularity. With longer follow-up, however, polyethylene "backside" wear and osteolysis are increased.
The best data on polyethylene wear and osteolysis has been reported in the all polyethylene total condylar prosthesis,[7,8] the one piece molded metal backed IB-1 prosthesis[9] and the compression molded one piece metal backed ACG prosthesis.[10] Currently on e the AGC total knee system is being manufactured.
Chitranjan S. Ranawat, MD,[11] described his 20-year follow-up study of 220 all polyethylene total condylar prostheses. At 20-years, 20 had been revised--4 for infection, 3 for fracture, and 13 for loosening. There were no cases of osteolysis. This study presents a good case for the all-polyethylene tibial component.
Ranawat[11] also reported on a prospectively randomized 180 press-fit condylar modular versus all-polyethylene tibial components performed between 1992 and 1994. At a mean follow-up of 6 years, 5 cases in the metal-backed group underwent revision for osteolysis compared with 0 cases in the all polyethylene group (P<.05). In all cases of revision for osteolysis, there was failure of the locking mechanism and "backside" wear.
In Ranawat's opinion, improvement in the locking mechanism between the tibial polyethylene insert and the metal tibial tray is imperative to reducing the incidence of osteolysis in cemented TKA. In the meantime, he considers preferable the components of molded or newer wear-resistance polyethylene (all poly) or molded, newer polyethylene components mechanically locked during manufacture to the metal tibial tray.
Results With an Epicondylar Axis Knee
Lawrence G. Morawa, MD[12] described a retrospective analysis of 50 consecutive posterior, stabilized, demented, tricompartmental total knee replacements with a minimum follow-up of 2 years. After surgery, the average range of motion was increased from 86° to 118° flexion. All patients had improved postoperative SF-36 scores. Pain and stair climbing function improved dramatically, and there were no revisions or infections. Nonprogressive radiolucent lines were present at the cement interface of the medial tibial bone in 10% of the tibial radiographs because of sclerotic subcondyle bone. After 2 years, overall Knee Society scores were excellent in 83% and good in 17% of patients, with a mean total score of 96 points.
References
1. Borden. Results of Porous coated total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
2. Elbert K, Bartel D, Wright T. The effect of conformity on stresses in dome-shaped polyethylene patellar components. Clin Orthop. 1995; 317:71-75.
3. Fehring TK, McAvoy G. Fluoroscopic evaluation of the painful total knee arthroplasty. Clin Orthop. 1996;331:226-233.
4. Epinette JA. Results with an HA coated total knee. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
5. Nilsson KG, Karrholm J, Carlsson L, Dalen T. Hydroxyapatite coating versus cemented fixation of the tibial component in total knee arthroplasty: prospective randomized comparison of hydroxyapatite-coated and cemented tibial components with 5-year follow-up using radiostereometry. J Arthroplasty. 1999;14:9-20.
6. Bartel DL, Burstein AH, Santavicco EA, Insall JN. Performance of the tibial component in total knee replacement. J Bone Joint Surg. 1982;64A:1026-1033.
7. Ranawat CS, Boachie-Adjei O Survivorship analysis and results of total condylar knee arthroplasty. Eight- to 11-year follow-up period. Clin Orthop 1988 Jan;(226):6-13.
8. Ranawat CS, Flynn WF Jr, Deshmukh RG Impact of modern technique on long-term results of total condylar knee arthroplasty. Clin Orthop 1994 Dec;(309):131-5
9. Font-Rodriguez DE, Scuderi GR, Insall JN: Survivorship of cemented total arthroplasty. Clin Orthop, 345:79-86, 1997.
10. Ritter MA, Worland R, Saliski J. Flat-on-flat, nonconstrained compression molded polyethylene total knee replacement. Clin Orthop 321:79-85, 1995.
11. Ranawat CS. Results with an all-poly tibial component. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
12. Morawa LG. Results with an epicondylar axis knee. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, James A. D'Antonio, MD, moderated a group of presentations on results of various designs in total knee arthroplasty (TKA).
Results of Porous Coated Total Knee Replacement
Lester S. Borden, MD,[1] acknowledged that cemented TKA is the "gold standard." Early designs of uncemented components were developed in an attempt to eliminate the need for cement and to prevent "cement disease." Surgeons wanted more stable bony ingrowth. Eventually "cement disease" was recognized as particle disease (mostly from polyethylene wear into crevices).
The original and most successful TKA, the porous coated anatomical (PCA) artificial total knee joints, were introduced in the early 1980s. These joints were designed for bony ingrowth and to provide for normal knee kinematics. The design also introduced modularity of the tibial components. To allow for more normal kinematics, the lack of constraint dictated a "flat-on-flat" design. This resulted in a very high rate of polyethylene wear and a revision rate of 10% per year. This design, however, contributed to the development of instrumentation for alignment of components.
Thin polyethylene, when subjected to high stresses, tends to wear excessively. This has been a major contributing factor to wear in all designs. Bartel and colleagues[2] examined polyethylene stresses in patellar components with convex-shaped articulating surfaces that contacted convex metallic surfaces. For patellar models, the von Mises stress was at or near the polyethylene yield stress in most of the contact area, which is consistent with the permanent deformation observed in many retrieved components. As such, deformation may continue, even when the component's surface has deformed and been worn into a concave shape.
Fehring and colleagues[3] evaluated 20 patients referred for pain and disability after TKA with fluoroscopy-guided radiographs. Fourteen of the 20 patients had radiolucent lines in their prostheses during this evaluation. All loose components as determined by fluoroscopy were confirmed on revision.
Fluoroscopy-guided radiographs can be helpful in evaluating the patient with a painful TKA and normal-appearing office radiographs. Newer uncemented total knee designs have improved anatomical shapes and contact areas and use screws for additional fixation. These enhancements have led to improved results with uncemented knee designs.
Results with an Hydroxyapatite-Coated Total Knee Design
Jean-Alain Epinette, MD,[4] opened by reviewing the prospective randomized analysis of Nilsson and colleagues[5] in which fixation of hydroxyapatite (HA)-coated designs in 29 knees were compared with cemented tibial components in 28 knees in the Tricon II TKA. Radiostereometric analysis revealed continuous migration of cemented components compared with slight unprogressive migration of HA-coated components. In the 40 patients (19 HA-coated, 21 cemented) remaining after 5 years, the HA-coated implants had most of their migration occurring within the initial 3 months but then stabilized, whereas the cemented implants showed an initially lower -- but over time continuously increasing -- migration.
Epinette's experience with 309 knees follow after a mean of 5 years (range 0 to 9 years) showed no mechanical failure in the femoral or tibial component. Eight of these knees required a repeated procedure for patella problems. Epinette found that HA filled in radiolucent gaps in follow-up radiographs.
Results With an All-Polyethylene Tibial Component
Evolution in TKA tibial component design has centered around metal tibial trays with improved stress transfer to the proximal tibia[6] and better fixation with pegs and cement. Benefits of metal tibial trays include durable fixation and modularity. With longer follow-up, however, polyethylene "backside" wear and osteolysis are increased.
The best data on polyethylene wear and osteolysis has been reported in the all polyethylene total condylar prosthesis,[7,8] the one piece molded metal backed IB-1 prosthesis[9] and the compression molded one piece metal backed ACG prosthesis.[10] Currently on e the AGC total knee system is being manufactured.
Chitranjan S. Ranawat, MD,[11] described his 20-year follow-up study of 220 all polyethylene total condylar prostheses. At 20-years, 20 had been revised--4 for infection, 3 for fracture, and 13 for loosening. There were no cases of osteolysis. This study presents a good case for the all-polyethylene tibial component.
Ranawat[11] also reported on a prospectively randomized 180 press-fit condylar modular versus all-polyethylene tibial components performed between 1992 and 1994. At a mean follow-up of 6 years, 5 cases in the metal-backed group underwent revision for osteolysis compared with 0 cases in the all polyethylene group (P<.05). In all cases of revision for osteolysis, there was failure of the locking mechanism and "backside" wear.
In Ranawat's opinion, improvement in the locking mechanism between the tibial polyethylene insert and the metal tibial tray is imperative to reducing the incidence of osteolysis in cemented TKA. In the meantime, he considers preferable the components of molded or newer wear-resistance polyethylene (all poly) or molded, newer polyethylene components mechanically locked during manufacture to the metal tibial tray.
Results With an Epicondylar Axis Knee
Lawrence G. Morawa, MD[12] described a retrospective analysis of 50 consecutive posterior, stabilized, demented, tricompartmental total knee replacements with a minimum follow-up of 2 years. After surgery, the average range of motion was increased from 86° to 118° flexion. All patients had improved postoperative SF-36 scores. Pain and stair climbing function improved dramatically, and there were no revisions or infections. Nonprogressive radiolucent lines were present at the cement interface of the medial tibial bone in 10% of the tibial radiographs because of sclerotic subcondyle bone. After 2 years, overall Knee Society scores were excellent in 83% and good in 17% of patients, with a mean total score of 96 points.
References
1. Borden. Results of Porous coated total knee replacement. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
2. Elbert K, Bartel D, Wright T. The effect of conformity on stresses in dome-shaped polyethylene patellar components. Clin Orthop. 1995; 317:71-75.
3. Fehring TK, McAvoy G. Fluoroscopic evaluation of the painful total knee arthroplasty. Clin Orthop. 1996;331:226-233.
4. Epinette JA. Results with an HA coated total knee. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
5. Nilsson KG, Karrholm J, Carlsson L, Dalen T. Hydroxyapatite coating versus cemented fixation of the tibial component in total knee arthroplasty: prospective randomized comparison of hydroxyapatite-coated and cemented tibial components with 5-year follow-up using radiostereometry. J Arthroplasty. 1999;14:9-20.
6. Bartel DL, Burstein AH, Santavicco EA, Insall JN. Performance of the tibial component in total knee replacement. J Bone Joint Surg. 1982;64A:1026-1033.
7. Ranawat CS, Boachie-Adjei O Survivorship analysis and results of total condylar knee arthroplasty. Eight- to 11-year follow-up period. Clin Orthop 1988 Jan;(226):6-13.
8. Ranawat CS, Flynn WF Jr, Deshmukh RG Impact of modern technique on long-term results of total condylar knee arthroplasty. Clin Orthop 1994 Dec;(309):131-5
9. Font-Rodriguez DE, Scuderi GR, Insall JN: Survivorship of cemented total arthroplasty. Clin Orthop, 345:79-86, 1997.
10. Ritter MA, Worland R, Saliski J. Flat-on-flat, nonconstrained compression molded polyethylene total knee replacement. Clin Orthop 321:79-85, 1995.
11. Ranawat CS. Results with an all-poly tibial component. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
12. Morawa LG. Results with an epicondylar axis knee. State of the Art Update in Orthopedics 2000. Whistler, BC: February 12-16, 2000.
Complications in Total Knee Arthroplasty
Donald T. Reilly, MD. PhD
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Lawrence G. Morawa, MD, moderated a group of presentations centered around the diagnosis and treatment of complications in total knee arthroplasty (TKA).
Diagnosing and Treating Infection
Although infection in total knee arthroplasty (TKA) is a relatively infrequent complication, it can be devastating in terms of morbidity and cost. Lester S. Borden, MD,[1] reviewed the diagnosis and treatment of infection in TKA. He began by stressing that this is a surgical disease. Long-term antibiotic depression is rarely indicated and is generally used only in patients for whom surgery is contraindicated.
Risk factors for knee infection include:
• multiple previous infections
• history of previous infection
• inflammatory arthritis (delayed infection)
• insulin dependent diabetes
• postthrombotic syndrome
• malnutrition.
Borden reviewed the importance of perioperative antibiotics. The institutional incidence of primary TKA infection should be around 1 %. Revision total knee replacement, however, carries at least a 2-fold increased risk for infection. In addition, late infections occur in approximately 2 per 1,000 TKAs annually.
Waldman and colleagues[2] retrospectively analyzed 290 patients with TKAs performed between 1982 and 1993 to define the risk for infection associated with dental surgery.
They identified 62 TKAs with late infections (occurring more than 6 months after procedure). Seven of these late infections were temporally and bacteriologically associated with dental procedures. Eight of 9 patients received no antibiotic prophylaxis. Fifty-six percent of the patients with late infections had positive risk factors, including diabetes and rheumatoid arthritis. These authors suggested prophylaxis for extensive dental work.
Diagnosing TKA infections is challenging, and prompt diagnosis and treatment are essential for a successful outcome. Windsor and colleagues[3] found that 96% of patients with infected TKAs presented with pain and 77 % had swelling. Only 27% had fever and drainage.
Treatment options for an infected TKA include:
• antibiotic suppression alone
• aggressive wound debridement, drainage, and antibiotic suppression therapy
• resection arthroplasty
• arthrodesis
• 2-stage reimplantation
• amputation.
The definitive diagnosis of infection is recovery of neutrophils by aspiration with greater than 30,000 leukocytes, 75% of which are polymorphonuclear. Five percent of infected TKAs in the Windsor study had negative cultures.
With an established infection, suppression is suggested only for patients in which surgery is not feasible. A low-virulence-organism, secure implant components, and well-tolerated oral antibiotics are required for cases in which suppression is chosen. Debridement with retention of the implant has a greater rate of success when there is meticulous synovectomy, copious irrigation, and parenteral antibiotics for 4 to 6 weeks in cases of acute infection.
According to Borden, management of infection with arthroscopy and multiple irrigations has yielded a lower rate of success. One-stage reimplantation, a more popular approach in Europe, may be possible for patients with acutely infected cementless TKAs and allows for debridement of the prosthesis-bone interface. Reimplantation usually requires antibiotic-impregnated cement. The gold standard for treatment of TKA infection remains the 2-stage reimplantation. This is especially successful in patients with chronically infected TKAs (ie, patients in whom symptoms persist for longer than 3 weeks.
Simmons and colleagues[4] performed a meta-analysis of 77 studies of 2-stage reimplantation and found an average success rate of 80%. This technique is more successful for cases of osteoarthritis with low-virulence bacteria and less successful for cases of rheumatoid arthritics and when high-virulence bacteria or multiple-organism infections are present. According to the Backe and colleagues,[5] a second 2-stage reimplantation following a failed 2-stage reimplantation has a success rate of approximately 80%.
There are few attractive surgical options for failed treatment of infected TKA. Arthrodesis should be considered when multiple surgical attempts fail to eradicate infection. Adequate bone stock, however, must be present for arthrodesis to be successful. Knee arthrodesis is challenging surgically and can be complicated by nonunion, malunion, or recurrent infection. A modular titanium intramedullary nail has been used in an attempt to reduce the incidence of nonunion and the rate of complications.
Waldman[6] reviewed the results of knee arthrodesis after infected TKA in 21 patients with a mean age of 64 years. Patients were followed for a mean of 2.4 years, and the mean number of previous operations was 4. Solid arthrodesis was achieved in 20 of 21 patients at approximately 6 months by using an intramedullary nail.
Borden discussed his personal approach to 2-stage reimplantation. His technique includes meticulous debridement with preservation of all noninvolved bone, preservation of collateral ligaments with resection of the posterior cruciate ligament, and the use of spacers (Prostalac). Prostalac remains interesting but controversial. He stressed the importance of skin closure. In the interval between removal and reimplantation, a patient should receive 4 to 6 weeks of intravenous antibiotics and no antibiotics for 1 to 2 weeks. An erythrocyte sedimentation rate and C-reactive protein test can be used to decide whether to reimplant. Borden emphasized the importance of antibiotics in cement used for reimplantation.
Looks Good, Feels Bad
Although the rate of dissatisfaction in patients with TKA is reported to be approximately less than 1%, evaluating a patient with pain or limited function is of utmost importance. James A. D'Antonio, MD,[7] reviewed the work-up of a patient with a painful or dysfunctional TKA.
D'Antonio presented a case of a 62-year-old active man who presented with pain. Plain radiographs and an examination appeared normal. However, slight rotation in several views other than ideal positioning showed loosening of an uncemented component. It is important to obtain fluoroscopic views if perfectly tangential radiographs of the prosthesis-bone interface are not available.
The second case was a 65-year-old man who reported that his knees were not supporting him. The examination revealed a very stable, well-aligned knee with no effusion. Radiographs showed no abnormalities. The patient had a history of alcoholism, which led to D'Antonio to the conclusion that the problem was with the patient not the arthroplasty. Evaluation of a patient who is unsatisfied with their
TKA should include:
• detailed history
• detailed physical examination, including chief complaints; pain; function; and neurovascular, psychosocial, and hip examinations
• radiographs and laboratory tests.
This work-up usually yields a diagnosis before surgery is necessary. D'Antonio stressed the importance of delaying surgery until the surgeon has reached a definitive diagnosis. Patients is key for surgeons encountering the small percentage of patients with TKA who are unhappy with unexplained pain or dysfunction.
Looks Bad, Feels Good
There are many failure mechanisms in TKA. These include:
• polyethylene wear
• instability
• aseptic Loosening
• extensor mechanism dysfunction
• unexplained pain
• infection.
George D. Markovich, MD,[8] examined the issue of "silent" osteolysis and the management of bone loss in TKA.
Femoral defects distally and posteriorly can be prevented with metal blocks on the femoral component to maintain the joint line.
Tibial wedges, half block, full block, and oblique full blocks are also useful.
Stems can be used enhance fixation when augments are used or bone quality is poor.
Markovich's presented his experience with 50 revision TKAs with metal augmentation followed for a maximum of 10 years.
To date, none of his patients treated with this technique have had failure of fixation of the components.
Osteolysis due to polyethylene wear may be present in patients with few symptoms. As such, patients often do not present with symptoms until after extensive structural damage has already occurred.
Early treatment is central to the prevention of widespread bone loss.
There are few data to guide the decision to intervene.
Regardless of whether a patient has osteolysis, the surgeon should continue to focus on the goals of restoration of bone stock, reestablishment of the joint line, and recreation of stability in the revision setting.
Lonner and colleagues[9] evaluated a total of 102 revision TKAs to determine the prodromal symptoms and radiographic findings associated with failure. The most important indicator for failure was pain, occurring in 84% of patients at an average of 13 months. Radiographs underestimated the diagnosis of osteolysis to be 4%. Osteolysis was confirmed during surgery in 22% of patients. The authors recommended an annual questionnaire and weight-bearing radiographs to ensure adequate surveillance of TKA patients.
Radiographs often underestimate the extent of bone loss. This inadequacy has prompted the development of more exact techniques, such as dual-energy x-ray absorptiometry and microradiographic evaluation, into the clinical setting. These techniques, however, remain experimental. Because of the shortcomings of radiographs in diagnosing osteolysis, the surgeon needs to be prepared for more than is preoperatively visible.
Markovich briefly discussed pharmaceutical intervention to prevent osteolysis. Shanbaga and colleagues[10] evaluated oral bisphosphonate therapy in a canine total hip replacement model. The dogs were randomized into 3 groups of 8, and a right uncemented total hip replacement was done on each animal. The control group (group 1) received no particulate debris. In groups 2 and 3, a mixture of fabricated ultra-high molecular weight polyethylene, titanium alloy, and cobalt chrome alloy was introduced into the proximal femoral gap. Group 3 also received a once-daily dose of 5 mg of alendronate sodium begun on day 7 and continued until the time of sacrifice.
Radiographically, 1 of 8 control dogs and 6 of 7 dogs from group 2 had periprosthetic radiolucencies with development of endosteal scalloping. In contrast, only 1 of 8 animals from group 3 had periprosthetic radiolucencies. Tissues from both experimental groups had significant macrophage infiltration. Levels of prostaglandin E2 and interleukin-1 were also significantly higher in the experimental groups than in controls. Continuous administration of alendronate effectively inhibited bone lysis for the 24-week duration of the study. Markovich stressed, however, that the clinical usefulness of this treatment is still in question.
Unstable Total Knee Replacement
Instability is the leading cause of failure in TKA.
A patient with preoperative ligament dyslaxity requires prosthetic substitution.
In patients with a primary TKA, a knee that is unbalanced after surgery was not balanced properly during surgery.
Secondary instability after surgery may result from after delayed rupture, wear, or loosening.
Patient history and clinical findings are important in the diagnosis of instability.
Radiographs are not usually helpful. Presentation usually takes the form of dissatisfaction with the knee, multiple falls, instability, pain, and effusion.
Patients are not usually cognizant of instability and usually describe situations in which they descend ramps and their knee tends to give way. Instability must be looked for in flexion, extension, and both positions (global instability).
References
• Borden LS. Diagnosing and treating infection. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Waldman BJ, Mont MA, Hungerford DS. Total knee arthroplasty infections associated with dental procedures. Clin Orthop. 1997;343:164-72.
• Windsor RE, Bono JV. Infected total knee replacements. J Am Acad Orthop Surg. 1994 Jan;2:44-53.
• Simmons TD, Stern SH. Diagnosis and management of the infected total knee arthroplasty. Am J Knee Surg. 1996;9:99-106.
• Backe HA Jr, Wolff DA, Windsor RE. Total knee replacement infection after 2-stage reimplantation: results of subsequent 2-stage reimplantation. Clin Orthop. 1996; 331:125-31.
• Waldman BJ, Mont MA, Payman KR, et al. Infected total knee arthroplasty treated with arthrodesis using a modular nail. Clin Orthop. 1999;367:230-7.
• D'Antonio J. Looks good, feels bad. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Markovich GD. Looks bad, feels good. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Lonner JH, Siliski JM, Scott RD. Prodromes of failure in total knee arthroplasty. J Arthroplasty. 1999;14:488.
• Shanbhag AS, Hasselman CT, Rubash HE. Inhibition of wear debris mediated osteolysis in a canine total hip arthroplasty model. Clin Orthop. 1997;344:33-43.
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Lawrence G. Morawa, MD, moderated a group of presentations centered around the diagnosis and treatment of complications in total knee arthroplasty (TKA).
Diagnosing and Treating Infection
Although infection in total knee arthroplasty (TKA) is a relatively infrequent complication, it can be devastating in terms of morbidity and cost. Lester S. Borden, MD,[1] reviewed the diagnosis and treatment of infection in TKA. He began by stressing that this is a surgical disease. Long-term antibiotic depression is rarely indicated and is generally used only in patients for whom surgery is contraindicated.
Risk factors for knee infection include:
• multiple previous infections
• history of previous infection
• inflammatory arthritis (delayed infection)
• insulin dependent diabetes
• postthrombotic syndrome
• malnutrition.
Borden reviewed the importance of perioperative antibiotics. The institutional incidence of primary TKA infection should be around 1 %. Revision total knee replacement, however, carries at least a 2-fold increased risk for infection. In addition, late infections occur in approximately 2 per 1,000 TKAs annually.
Waldman and colleagues[2] retrospectively analyzed 290 patients with TKAs performed between 1982 and 1993 to define the risk for infection associated with dental surgery.
They identified 62 TKAs with late infections (occurring more than 6 months after procedure). Seven of these late infections were temporally and bacteriologically associated with dental procedures. Eight of 9 patients received no antibiotic prophylaxis. Fifty-six percent of the patients with late infections had positive risk factors, including diabetes and rheumatoid arthritis. These authors suggested prophylaxis for extensive dental work.
Diagnosing TKA infections is challenging, and prompt diagnosis and treatment are essential for a successful outcome. Windsor and colleagues[3] found that 96% of patients with infected TKAs presented with pain and 77 % had swelling. Only 27% had fever and drainage.
Treatment options for an infected TKA include:
• antibiotic suppression alone
• aggressive wound debridement, drainage, and antibiotic suppression therapy
• resection arthroplasty
• arthrodesis
• 2-stage reimplantation
• amputation.
The definitive diagnosis of infection is recovery of neutrophils by aspiration with greater than 30,000 leukocytes, 75% of which are polymorphonuclear. Five percent of infected TKAs in the Windsor study had negative cultures.
With an established infection, suppression is suggested only for patients in which surgery is not feasible. A low-virulence-organism, secure implant components, and well-tolerated oral antibiotics are required for cases in which suppression is chosen. Debridement with retention of the implant has a greater rate of success when there is meticulous synovectomy, copious irrigation, and parenteral antibiotics for 4 to 6 weeks in cases of acute infection.
According to Borden, management of infection with arthroscopy and multiple irrigations has yielded a lower rate of success. One-stage reimplantation, a more popular approach in Europe, may be possible for patients with acutely infected cementless TKAs and allows for debridement of the prosthesis-bone interface. Reimplantation usually requires antibiotic-impregnated cement. The gold standard for treatment of TKA infection remains the 2-stage reimplantation. This is especially successful in patients with chronically infected TKAs (ie, patients in whom symptoms persist for longer than 3 weeks.
Simmons and colleagues[4] performed a meta-analysis of 77 studies of 2-stage reimplantation and found an average success rate of 80%. This technique is more successful for cases of osteoarthritis with low-virulence bacteria and less successful for cases of rheumatoid arthritics and when high-virulence bacteria or multiple-organism infections are present. According to the Backe and colleagues,[5] a second 2-stage reimplantation following a failed 2-stage reimplantation has a success rate of approximately 80%.
There are few attractive surgical options for failed treatment of infected TKA. Arthrodesis should be considered when multiple surgical attempts fail to eradicate infection. Adequate bone stock, however, must be present for arthrodesis to be successful. Knee arthrodesis is challenging surgically and can be complicated by nonunion, malunion, or recurrent infection. A modular titanium intramedullary nail has been used in an attempt to reduce the incidence of nonunion and the rate of complications.
Waldman[6] reviewed the results of knee arthrodesis after infected TKA in 21 patients with a mean age of 64 years. Patients were followed for a mean of 2.4 years, and the mean number of previous operations was 4. Solid arthrodesis was achieved in 20 of 21 patients at approximately 6 months by using an intramedullary nail.
Borden discussed his personal approach to 2-stage reimplantation. His technique includes meticulous debridement with preservation of all noninvolved bone, preservation of collateral ligaments with resection of the posterior cruciate ligament, and the use of spacers (Prostalac). Prostalac remains interesting but controversial. He stressed the importance of skin closure. In the interval between removal and reimplantation, a patient should receive 4 to 6 weeks of intravenous antibiotics and no antibiotics for 1 to 2 weeks. An erythrocyte sedimentation rate and C-reactive protein test can be used to decide whether to reimplant. Borden emphasized the importance of antibiotics in cement used for reimplantation.
Looks Good, Feels Bad
Although the rate of dissatisfaction in patients with TKA is reported to be approximately less than 1%, evaluating a patient with pain or limited function is of utmost importance. James A. D'Antonio, MD,[7] reviewed the work-up of a patient with a painful or dysfunctional TKA.
D'Antonio presented a case of a 62-year-old active man who presented with pain. Plain radiographs and an examination appeared normal. However, slight rotation in several views other than ideal positioning showed loosening of an uncemented component. It is important to obtain fluoroscopic views if perfectly tangential radiographs of the prosthesis-bone interface are not available.
The second case was a 65-year-old man who reported that his knees were not supporting him. The examination revealed a very stable, well-aligned knee with no effusion. Radiographs showed no abnormalities. The patient had a history of alcoholism, which led to D'Antonio to the conclusion that the problem was with the patient not the arthroplasty. Evaluation of a patient who is unsatisfied with their
TKA should include:
• detailed history
• detailed physical examination, including chief complaints; pain; function; and neurovascular, psychosocial, and hip examinations
• radiographs and laboratory tests.
This work-up usually yields a diagnosis before surgery is necessary. D'Antonio stressed the importance of delaying surgery until the surgeon has reached a definitive diagnosis. Patients is key for surgeons encountering the small percentage of patients with TKA who are unhappy with unexplained pain or dysfunction.
Looks Bad, Feels Good
There are many failure mechanisms in TKA. These include:
• polyethylene wear
• instability
• aseptic Loosening
• extensor mechanism dysfunction
• unexplained pain
• infection.
George D. Markovich, MD,[8] examined the issue of "silent" osteolysis and the management of bone loss in TKA.
Femoral defects distally and posteriorly can be prevented with metal blocks on the femoral component to maintain the joint line.
Tibial wedges, half block, full block, and oblique full blocks are also useful.
Stems can be used enhance fixation when augments are used or bone quality is poor.
Markovich's presented his experience with 50 revision TKAs with metal augmentation followed for a maximum of 10 years.
To date, none of his patients treated with this technique have had failure of fixation of the components.
Osteolysis due to polyethylene wear may be present in patients with few symptoms. As such, patients often do not present with symptoms until after extensive structural damage has already occurred.
Early treatment is central to the prevention of widespread bone loss.
There are few data to guide the decision to intervene.
Regardless of whether a patient has osteolysis, the surgeon should continue to focus on the goals of restoration of bone stock, reestablishment of the joint line, and recreation of stability in the revision setting.
Lonner and colleagues[9] evaluated a total of 102 revision TKAs to determine the prodromal symptoms and radiographic findings associated with failure. The most important indicator for failure was pain, occurring in 84% of patients at an average of 13 months. Radiographs underestimated the diagnosis of osteolysis to be 4%. Osteolysis was confirmed during surgery in 22% of patients. The authors recommended an annual questionnaire and weight-bearing radiographs to ensure adequate surveillance of TKA patients.
Radiographs often underestimate the extent of bone loss. This inadequacy has prompted the development of more exact techniques, such as dual-energy x-ray absorptiometry and microradiographic evaluation, into the clinical setting. These techniques, however, remain experimental. Because of the shortcomings of radiographs in diagnosing osteolysis, the surgeon needs to be prepared for more than is preoperatively visible.
Markovich briefly discussed pharmaceutical intervention to prevent osteolysis. Shanbaga and colleagues[10] evaluated oral bisphosphonate therapy in a canine total hip replacement model. The dogs were randomized into 3 groups of 8, and a right uncemented total hip replacement was done on each animal. The control group (group 1) received no particulate debris. In groups 2 and 3, a mixture of fabricated ultra-high molecular weight polyethylene, titanium alloy, and cobalt chrome alloy was introduced into the proximal femoral gap. Group 3 also received a once-daily dose of 5 mg of alendronate sodium begun on day 7 and continued until the time of sacrifice.
Radiographically, 1 of 8 control dogs and 6 of 7 dogs from group 2 had periprosthetic radiolucencies with development of endosteal scalloping. In contrast, only 1 of 8 animals from group 3 had periprosthetic radiolucencies. Tissues from both experimental groups had significant macrophage infiltration. Levels of prostaglandin E2 and interleukin-1 were also significantly higher in the experimental groups than in controls. Continuous administration of alendronate effectively inhibited bone lysis for the 24-week duration of the study. Markovich stressed, however, that the clinical usefulness of this treatment is still in question.
Unstable Total Knee Replacement
Instability is the leading cause of failure in TKA.
A patient with preoperative ligament dyslaxity requires prosthetic substitution.
In patients with a primary TKA, a knee that is unbalanced after surgery was not balanced properly during surgery.
Secondary instability after surgery may result from after delayed rupture, wear, or loosening.
Patient history and clinical findings are important in the diagnosis of instability.
Radiographs are not usually helpful. Presentation usually takes the form of dissatisfaction with the knee, multiple falls, instability, pain, and effusion.
Patients are not usually cognizant of instability and usually describe situations in which they descend ramps and their knee tends to give way. Instability must be looked for in flexion, extension, and both positions (global instability).
References
• Borden LS. Diagnosing and treating infection. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Waldman BJ, Mont MA, Hungerford DS. Total knee arthroplasty infections associated with dental procedures. Clin Orthop. 1997;343:164-72.
• Windsor RE, Bono JV. Infected total knee replacements. J Am Acad Orthop Surg. 1994 Jan;2:44-53.
• Simmons TD, Stern SH. Diagnosis and management of the infected total knee arthroplasty. Am J Knee Surg. 1996;9:99-106.
• Backe HA Jr, Wolff DA, Windsor RE. Total knee replacement infection after 2-stage reimplantation: results of subsequent 2-stage reimplantation. Clin Orthop. 1996; 331:125-31.
• Waldman BJ, Mont MA, Payman KR, et al. Infected total knee arthroplasty treated with arthrodesis using a modular nail. Clin Orthop. 1999;367:230-7.
• D'Antonio J. Looks good, feels bad. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Markovich GD. Looks bad, feels good. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.
• Lonner JH, Siliski JM, Scott RD. Prodromes of failure in total knee arthroplasty. J Arthroplasty. 1999;14:488.
• Shanbhag AS, Hasselman CT, Rubash HE. Inhibition of wear debris mediated osteolysis in a canine total hip arthroplasty model. Clin Orthop. 1997;344:33-43.
Challenges in Total Knee Replacement
Donald T. Reilly, MD. PhD
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Anthony K. Hedley, MD, moderated a group of presentations on challenges in total knee arthroplasty (TKA), ranging from patellar clunk syndrome to the dislocated patella/extensor mechanism.
Patellar Clunk Syndrome
Excellent results have been reported with posterior stabilized TKA. A common complication relating to patellofemoral articulation, however, is patellar clunk syndrome. This syndrome is the painful crepitus under the quadriceps tendon at the anterior knee that is caused by soft tissue catching in the intercondylar notch of the femoral component. A fibrous nodule (hypertropic scar tissue) forms on the quadriceps tendon proximal to the patellar replacement and causes pain. George D. Markovich, MD,[1] examined the many factors involved in patellar clunk syndrome and its treatment options.
Although the cause of patellar clunk syndrome is still being determined, it probably results from a combination of implant design, patient characteristics, and surgical technique. Other issues that contribute to the development of this syndrome include notch and trochlear design, raised joint line, rotational malalignment of the tibiofemoral articulation, and superior patellar overhang.
Treatment options for the syndrome includes:
• nonsteroidal anti-inflammatory medications
• arthroscopic debridement down to the quadriceps tendon
• open synovectomy for correction of implant problems.
To prevent or reduce the incidence of patellar clunk syndrome, the implant design should be smooth from the condyles to the trochlear groove. This syndrome is more common in posterior-stabilized designs. In a prospective, randomized study, Jankiewicz and colleagues[2] found this syndrome in 2% to 3% of patients with Insall-Burstein posterior stabilized TKAs.
Lucas and colleague[3] evaluated 32 knees in 30 consecutive patients diagnosed with patellar clunk syndrome at 1 year after arthroscopic debridement through a superolateral portal. Patients were diagnosed with the syndrome an average of 12 months after their most recent knee arthroplasty. All patients treated had been free of the syndrome after surgery, although 1 patient reported persistent anterior knee pain. Knee Society scores increased from an average of 64 points to 93 points after surgery.
Exposure of the Tight Knee
Donald T. Reilly, MD, reviewed exposure of the tight knee after TKA. He emphasized the importance of the skin incision. Tight knees that have undergone several procedures often have multiple incisions. As such, a sham incision is recommended, and surgeons should include previous incisions in the current one.
Mobilization of the patella is important in the tight knee. Recreation of the medial and lateral gutters allows this mobilization. A patellar-femoral ligament release aids in exposure of the lateral knee. With severe obesity and a thickened cutaneous flap, the patella should be turned in a prepatella Bursal pocket. Exposure can be enhanced by the quadriceps snip, quadriceps turn-down, and tubercle osteotomy. Reilly stressed the importance of bone quality and fragment size (at least 6 to 7 cm in length) in the tibia tubercle osteotomy. A proximal tibial shelf should be formed to prevent migration. Various options for fixation exist, including those involving screws and wires.
The Dislocated Patella/Extensor Mechanism
Kenneth A. Krackow, MD,[5] examined patellar dislocation in TKA. According to a study by Ewald and colleagues[6] on 192 kinematic TKAs, the incidence of patella dislocation is approximately 0.65%.
There are two types of dislocation: extension and flexion. Both types of dislocation can be attributed to a weak vastus medialis oblicus. The extension type depends on the design of the prosthetic trochlear groove and valgus orientation of the femoral component. If varus is placed in the tibial cut, to obtain overall valgus alignment excessive valgus position of the femoral component (increased Q angle) occurs and capture of the patella in extension is made difficult. Because it is mostly a dynamic muscular balance problem, extension-type dislocation is difficult to detect in surgery and can be impossible to detect in a paralyzed patient.
Flexion is the more common type of dislocation. It too is exacerbated by an increased Q angle. Other causes of flexion are overstuffing of the patellar-femoral joint, femoral component malrotation, poor capture in congruent design-type components, and a poorly done patella bony cut.
Minor subluxation can be treated with valgus release but complete dislocation usually requires tibial tubercle medialization without distallization. Krackow described his personal experience of 22 knees in 19 patients in which tibial tubercle medialization corrected dislocation of the patella.
References
1. Markovich GD. Patellar clunk syndrome. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.2. Jankiewicz JJ. A prospective, randomized study of patellofemoral complications in two posterior cruciate-substituting total knee systems. Eastern Orthopaedic Association Meeting; 1995.
2. Lucas TS, DeLuca PF, Nazarian DG, Bartolozzi AR, Booth RE Jr. Arthroscopic treatment of patellar clunk. Clin Orthop. 1999;367:226-9.
3. Reilly DT. Exposure of the tight knee. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
4. Krackow KA. The dislocated patella/extensor mechanism. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
5. Wright J, Ewald FC, Walker PS, Thomas WH, Poss R, Sledge CB. Total knee arthroplasty with the kinematic prosthesis. Results after five to nine years: a follow-up note. J Bone Joint Surg Am .1990;Aug;72:1003-1009.
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Anthony K. Hedley, MD, moderated a group of presentations on challenges in total knee arthroplasty (TKA), ranging from patellar clunk syndrome to the dislocated patella/extensor mechanism.
Patellar Clunk Syndrome
Excellent results have been reported with posterior stabilized TKA. A common complication relating to patellofemoral articulation, however, is patellar clunk syndrome. This syndrome is the painful crepitus under the quadriceps tendon at the anterior knee that is caused by soft tissue catching in the intercondylar notch of the femoral component. A fibrous nodule (hypertropic scar tissue) forms on the quadriceps tendon proximal to the patellar replacement and causes pain. George D. Markovich, MD,[1] examined the many factors involved in patellar clunk syndrome and its treatment options.
Although the cause of patellar clunk syndrome is still being determined, it probably results from a combination of implant design, patient characteristics, and surgical technique. Other issues that contribute to the development of this syndrome include notch and trochlear design, raised joint line, rotational malalignment of the tibiofemoral articulation, and superior patellar overhang.
Treatment options for the syndrome includes:
• nonsteroidal anti-inflammatory medications
• arthroscopic debridement down to the quadriceps tendon
• open synovectomy for correction of implant problems.
To prevent or reduce the incidence of patellar clunk syndrome, the implant design should be smooth from the condyles to the trochlear groove. This syndrome is more common in posterior-stabilized designs. In a prospective, randomized study, Jankiewicz and colleagues[2] found this syndrome in 2% to 3% of patients with Insall-Burstein posterior stabilized TKAs.
Lucas and colleague[3] evaluated 32 knees in 30 consecutive patients diagnosed with patellar clunk syndrome at 1 year after arthroscopic debridement through a superolateral portal. Patients were diagnosed with the syndrome an average of 12 months after their most recent knee arthroplasty. All patients treated had been free of the syndrome after surgery, although 1 patient reported persistent anterior knee pain. Knee Society scores increased from an average of 64 points to 93 points after surgery.
Exposure of the Tight Knee
Donald T. Reilly, MD, reviewed exposure of the tight knee after TKA. He emphasized the importance of the skin incision. Tight knees that have undergone several procedures often have multiple incisions. As such, a sham incision is recommended, and surgeons should include previous incisions in the current one.
Mobilization of the patella is important in the tight knee. Recreation of the medial and lateral gutters allows this mobilization. A patellar-femoral ligament release aids in exposure of the lateral knee. With severe obesity and a thickened cutaneous flap, the patella should be turned in a prepatella Bursal pocket. Exposure can be enhanced by the quadriceps snip, quadriceps turn-down, and tubercle osteotomy. Reilly stressed the importance of bone quality and fragment size (at least 6 to 7 cm in length) in the tibia tubercle osteotomy. A proximal tibial shelf should be formed to prevent migration. Various options for fixation exist, including those involving screws and wires.
The Dislocated Patella/Extensor Mechanism
Kenneth A. Krackow, MD,[5] examined patellar dislocation in TKA. According to a study by Ewald and colleagues[6] on 192 kinematic TKAs, the incidence of patella dislocation is approximately 0.65%.
There are two types of dislocation: extension and flexion. Both types of dislocation can be attributed to a weak vastus medialis oblicus. The extension type depends on the design of the prosthetic trochlear groove and valgus orientation of the femoral component. If varus is placed in the tibial cut, to obtain overall valgus alignment excessive valgus position of the femoral component (increased Q angle) occurs and capture of the patella in extension is made difficult. Because it is mostly a dynamic muscular balance problem, extension-type dislocation is difficult to detect in surgery and can be impossible to detect in a paralyzed patient.
Flexion is the more common type of dislocation. It too is exacerbated by an increased Q angle. Other causes of flexion are overstuffing of the patellar-femoral joint, femoral component malrotation, poor capture in congruent design-type components, and a poorly done patella bony cut.
Minor subluxation can be treated with valgus release but complete dislocation usually requires tibial tubercle medialization without distallization. Krackow described his personal experience of 22 knees in 19 patients in which tibial tubercle medialization corrected dislocation of the patella.
References
1. Markovich GD. Patellar clunk syndrome. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16.2. Jankiewicz JJ. A prospective, randomized study of patellofemoral complications in two posterior cruciate-substituting total knee systems. Eastern Orthopaedic Association Meeting; 1995.
2. Lucas TS, DeLuca PF, Nazarian DG, Bartolozzi AR, Booth RE Jr. Arthroscopic treatment of patellar clunk. Clin Orthop. 1999;367:226-9.
3. Reilly DT. Exposure of the tight knee. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
4. Krackow KA. The dislocated patella/extensor mechanism. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
5. Wright J, Ewald FC, Walker PS, Thomas WH, Poss R, Sledge CB. Total knee arthroplasty with the kinematic prosthesis. Results after five to nine years: a follow-up note. J Bone Joint Surg Am .1990;Aug;72:1003-1009.
Basic Science Issues in Primary Total Knee Replacement
Donald T. Reilly, MD. PhD
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Kenneth A. Krakow, MD, moderated a group of presentations on the anatomy and biomechanics of total knee arthroplasty (TKA).
Anatomy and Biomechanics of the Normal Knee
Donald T. Reilly, MD, PhD,[1] explained the importance of incorporating normal knee kinematics into total knee designs. The historical anatomical orthogonal approach to knee kinematics induces the "J-curve," or the instant center of rotation of the knee. Brunet and colleagues[2] have demonstrated that analysis using the mechanical axis to orient the plane of rotation produces a signal point that defines the instant center of rotation as the epicondylar axis. This simplifies prosthetic design because a single radius can be used in the prosthesis for flexion and extension of the knee. This also simplifies manufacture and may eliminate mid-flexion instability. Designs based on the "J-curve" would be expected to produce better kinematics if placed in anatomical position rather than in the externally rotated femoral position. With a single axis of rotation kept more posterior, the momentum for the extension mechanism is enhanced and stair climbing and rising from a chair may be improved.
Biological Analysis of Retrieved Total Knee Arthroplasties
Thomas W. Bauer, MD, PhD,[3] discussed the benefits of analyzing retrieved TKAs. Retrieval analysis allows investigators to determine whether the design goals of the arthroplasty have been met in the clinical setting. Bauer first described levels of ingrowth in uncemented knees. Ingrowth has been shown in the past to occur in 10% to 29% of uncemented tibiae. Dr. Bauer presented retrieval data from a 59-year-old woman with rheumatoid arthritis who died subsequent to a well-functioning TKA. The analysis for ingrowth with both coronal and sagittal sections of the specimen showed less than 5% ingrowth of the entire surface area. This small amount of bony ingrowth implies that channels allow debris to contact the bone-prosthesis interface and cause osteolysis.
In retrieval studies, differentiation between wear and deformation is difficult. Bauer presented his own analysis of "backside wear" on 105 retrieved tibial inserts of multiple designs.[3] A total of 22 inserts showed evidence of backside wear, whereas many more showed evidence of deformation. However, creep cannot be considered as wear. Thirty-one inserts showed eccentric patterns of wear; these patterns were more common in retained typed replacements of the posterior cruciate ligament. Bauer pointed out that the retrievals were from revisions and not necessarily from well-functioning total knee replacements. The high backside wear was attributed to thin polyethylene, high articular surface wear, and length of time in vivo. These studies question the clinical significance of backside wear.
Does Contact Area Matter?
Traditionally, TKA designs have focused on increasing surface area of contact to decrease stresses at the articulation. Avram A. Edidin, PhD,[4] challenged the dictum that contact area is the all-important variable in TKA wear.
Retrieved degraded tibial components have the appearance of "case-hardened failure," in which the predominant failure mechanisms are spalling and galling. These failure mechanisms result more from degradation than from stress. To investigate these mechanisms, Edidin developed a small punch test that causes multiaxial loading similar to that which occurs in the polyethylene of TKAs. This test can retrieve small specimens throughout the thickness of a polyethylene insert and shows that degraded areas occur in the subsurface region where stresses (regardless of conformity) are highest. Sterilization of the material in inert atmospheres decreases degradation and enhances resistance to stresses. These experiments postulate that degradation rather than stress is the primary reason for delamination in TKA.
Osteotomy-Unicondylar Replacement
Peter M. Bonutti, MD,[5] outlined the complexities facing orthopedic surgeons choosing the best procedure for TKA in patients with unicompartmental osteoarthritis. Tibial osteotomy is favored for the younger, highly active patient with good range of motion and a normal patellar-femoral joint. Contraindications to this procedure include multiple compartment involvement and inflammatory disease. Unless a closing wedge procedure is prevented by ligament laxity, Bonutti favors this procedure over the opening wedge procedure because of the higher complication rate secondary to device failure and graft collapse in the open wedge procedure. Although osteotomy has poor long-term results, it can "buy time" for younger patients to perform more strenuous activities and postpone the need for arthroplasty.
The ideal patient for unicondylar replacement is an older, thinner patient with good range of motion and lower activity levels. This type of arthroplasty requires adequate function of all ligaments and minimal deformity to achieve the highest success rate. Disadvantages of the procedure include the small number of patients who fulfill this criteria and the resulting lack of experience with the procedure for orthopedic surgeons coupled its level of difficulty.
TKA remains the gold standard for elderly patients. This procedure yields the most reliable pain relief and longevity in patients with full compartment involvement, poor range of motion, ligament instability, and severe deformity.
References
1. Reilly DT. Anatomy and biomechanics of the normal knee. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
2. Brunet ME, Kester MA, Cook SD, Haddad RJ, Skinner HB. Determination of the transverse centre of rotation of the knee using CAT scans. Eng Med. 1986;15:143-7.
3. Bauer TW. Biological analysis of retrieved total knees. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
4. Edidin AA. Does contact area matter? State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
5. Bonutti PM. Osteotomy-unicondylar replacement-total knee replacement. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
Introduction
At the recent State of the Art Update in Orthopaedics 2000 in Whistler, British Columbia, Kenneth A. Krakow, MD, moderated a group of presentations on the anatomy and biomechanics of total knee arthroplasty (TKA).
Anatomy and Biomechanics of the Normal Knee
Donald T. Reilly, MD, PhD,[1] explained the importance of incorporating normal knee kinematics into total knee designs. The historical anatomical orthogonal approach to knee kinematics induces the "J-curve," or the instant center of rotation of the knee. Brunet and colleagues[2] have demonstrated that analysis using the mechanical axis to orient the plane of rotation produces a signal point that defines the instant center of rotation as the epicondylar axis. This simplifies prosthetic design because a single radius can be used in the prosthesis for flexion and extension of the knee. This also simplifies manufacture and may eliminate mid-flexion instability. Designs based on the "J-curve" would be expected to produce better kinematics if placed in anatomical position rather than in the externally rotated femoral position. With a single axis of rotation kept more posterior, the momentum for the extension mechanism is enhanced and stair climbing and rising from a chair may be improved.
Biological Analysis of Retrieved Total Knee Arthroplasties
Thomas W. Bauer, MD, PhD,[3] discussed the benefits of analyzing retrieved TKAs. Retrieval analysis allows investigators to determine whether the design goals of the arthroplasty have been met in the clinical setting. Bauer first described levels of ingrowth in uncemented knees. Ingrowth has been shown in the past to occur in 10% to 29% of uncemented tibiae. Dr. Bauer presented retrieval data from a 59-year-old woman with rheumatoid arthritis who died subsequent to a well-functioning TKA. The analysis for ingrowth with both coronal and sagittal sections of the specimen showed less than 5% ingrowth of the entire surface area. This small amount of bony ingrowth implies that channels allow debris to contact the bone-prosthesis interface and cause osteolysis.
In retrieval studies, differentiation between wear and deformation is difficult. Bauer presented his own analysis of "backside wear" on 105 retrieved tibial inserts of multiple designs.[3] A total of 22 inserts showed evidence of backside wear, whereas many more showed evidence of deformation. However, creep cannot be considered as wear. Thirty-one inserts showed eccentric patterns of wear; these patterns were more common in retained typed replacements of the posterior cruciate ligament. Bauer pointed out that the retrievals were from revisions and not necessarily from well-functioning total knee replacements. The high backside wear was attributed to thin polyethylene, high articular surface wear, and length of time in vivo. These studies question the clinical significance of backside wear.
Does Contact Area Matter?
Traditionally, TKA designs have focused on increasing surface area of contact to decrease stresses at the articulation. Avram A. Edidin, PhD,[4] challenged the dictum that contact area is the all-important variable in TKA wear.
Retrieved degraded tibial components have the appearance of "case-hardened failure," in which the predominant failure mechanisms are spalling and galling. These failure mechanisms result more from degradation than from stress. To investigate these mechanisms, Edidin developed a small punch test that causes multiaxial loading similar to that which occurs in the polyethylene of TKAs. This test can retrieve small specimens throughout the thickness of a polyethylene insert and shows that degraded areas occur in the subsurface region where stresses (regardless of conformity) are highest. Sterilization of the material in inert atmospheres decreases degradation and enhances resistance to stresses. These experiments postulate that degradation rather than stress is the primary reason for delamination in TKA.
Osteotomy-Unicondylar Replacement
Peter M. Bonutti, MD,[5] outlined the complexities facing orthopedic surgeons choosing the best procedure for TKA in patients with unicompartmental osteoarthritis. Tibial osteotomy is favored for the younger, highly active patient with good range of motion and a normal patellar-femoral joint. Contraindications to this procedure include multiple compartment involvement and inflammatory disease. Unless a closing wedge procedure is prevented by ligament laxity, Bonutti favors this procedure over the opening wedge procedure because of the higher complication rate secondary to device failure and graft collapse in the open wedge procedure. Although osteotomy has poor long-term results, it can "buy time" for younger patients to perform more strenuous activities and postpone the need for arthroplasty.
The ideal patient for unicondylar replacement is an older, thinner patient with good range of motion and lower activity levels. This type of arthroplasty requires adequate function of all ligaments and minimal deformity to achieve the highest success rate. Disadvantages of the procedure include the small number of patients who fulfill this criteria and the resulting lack of experience with the procedure for orthopedic surgeons coupled its level of difficulty.
TKA remains the gold standard for elderly patients. This procedure yields the most reliable pain relief and longevity in patients with full compartment involvement, poor range of motion, ligament instability, and severe deformity.
References
1. Reilly DT. Anatomy and biomechanics of the normal knee. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
2. Brunet ME, Kester MA, Cook SD, Haddad RJ, Skinner HB. Determination of the transverse centre of rotation of the knee using CAT scans. Eng Med. 1986;15:143-7.
3. Bauer TW. Biological analysis of retrieved total knees. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
4. Edidin AA. Does contact area matter? State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.
5. Bonutti PM. Osteotomy-unicondylar replacement-total knee replacement. State of the Art Update in Orthopaedics 2000. Whistler, BC: February 12-16, 2000.