Floor Reaction Orthosis

FLOOR REACTION ORTHOSIS (FRO)

 Revolutionary orthoses: Custom fabricated, moulded plastic device that supports the ankle and foot area of the body and extends from below the knee down to and including the foot.

It was described by Saltiel for the use of weak quadriceps or plantar flexors in 1969

 It holds the ankle in equinus to prevent the heel from touching the ground. As the body weight brings the heel downwards, the suprapatellar band will press the knee back preventing knee from buckling during stance phase
 It allows the knee to flex during swing phase when the foot is off the ground

Use:
 It can be used in lower limb paralyses with weak quadriceps like post polio residual paralysis


Advantages over other AK Orthosis:
 Light weight-300gms
 Swing phase is not laboured
 Floor reaction prevents knee from buckling
 2 weeks training is enough to use it.
 Stabilises knee without muscle action
 Ground clearance is easier
 Good patient compliance
 Cosmetically acceptable-can be worn under shoe

Disadvantages:
 Must be correct fitting or else it wont function
 Has to be custom made

DNB Theory Paper 2009 December

DNB Orthopaedics Theory December 2009

Paper 1
1. Post-operative pain management. Describe patient control analgesia.
2. Clinical features and management of stove in chest.
3. Indications of Limb salvage surgery in malignant bone tumors. Describe the techniques of limb salvage in osteosarcoma.
4. Uses of botulinum neurotoxin in Orthopaedic surgery.
5. Define pigmented villonodular synovitis. Describe pathology, clinical features, diagnosis & its treatment.
6. Give a functional classification of muscles around the shoulder. Enumerate the indications for shoulder arthrodesis. What are the pre-requisites for a good result? Describe any one technique of shoulder arthrodesis.
7. Describe pathophysiology of nerve compression (entrapment) syndromes. Enumerate various syndromes of nerve entrapment. Give an outline of the management of Tarsal Tunnel Syndrome.
8. What is traumatic arthrotomy of the knee joint? What is fluid challenge test to confirm the diagnosis in doubtful cases? Outline the principles of management.
9. What are the various causes of late onset paraplegia in tuberculosis of spine? Describe the investigative modalities and outline the principles of management.
10. Describe the management of unicompartmental osteoarthrosis knee.

Paper 2
1. Management of septic arthritis in children,
2. Pathophysiology, types and clinical features of Osteogenesis Imperfecta
3. Prognostic factors and outcome in the treatment of Perthe’s disease
4. Describe Madelung deformity, classification, clinical features and management of madelung's deformity
5. Classify congenital dislocation of knee. Comment on differential diagnosis and management
6. Draw a diagram of Floor Reaction Orthosis, What is a good indication for its use. Describe mechanism of action
7. Orthopaedic manifestation of neurofibromatosis
8. Describe muscular dynamics in calcaneovalgus deformity. Describe management in patients before and after attaining skeletal maturity
9. Classification of neurogenic bladder and management
10. What are closed chain and open chain exercises and discuss ACL rehabilitation protocol


Paper 3
1. Classification, management and complication of fractures of the femoral head and neck in children
2. What are Monteggia equivalents, discuss the principles of management of Monteggia fracture dislocation in children
3. Principles of management of a pulseless hand after supracondylar fractures in children
4. Role of ultrasound in fracture healing
5. Subacromial impingement syndrome
6. Describe indications for amputation, Principles of lower limb amputation in children
7. What is Mangled Extremity severity score(MESS), describe principles of flap coverage in proximal one third of tibia
8. Classify ankle fractures, which pattern has syndesmotic instability, what is their management?
9. What are biodegradable implants, what is their chemical composition? Mention the indications of their use, advantage and disadvantage of their use
10. What is central cord syndrome, describe its clinical presentation. How will you manage such a case?

Paper 4
1. Osteochondral allograft transplantation. Mention indications for the procedure
2. Role of Pamidronate in bone metastasis
3. What do you understand by patellar instability, describe the principles of management, before and after skeletal maturity?
4. Enumerate modalities leading to biological enhancement of fracture healing. Mention the methods of preservation of allogenic bone grafts. Comment on mode of action, advantages and disadvantages
5. Describe the pathogenesis of hallux valgus deformity; describe the role of metatarsus primary varus in the pathogenesis. How will you manage an adolescent girl with severe hallux valgus?
6. Describe various types of rickets; describe biochemical changes and clinical presentation of various types of rickets!
7. Define osteoporosis. Comment on types, causes and management
8. What is highly cross linked polyethylene? How is it manufactured? How has it affected modern total hip arthroplasty?
9. Anatomy of Lisfranc joint, and management of injuries around the joint
10. Describe gate control theory of pain. What is transcutaneous nerve stimulation and its indications?

Parathormone(PTH)

Composition and Mechanism of action:

• Endogenous PTH is an 84-amino-acid peptide that is largely responsible for calcium homeostasis
• Although chronic elevation of PTH, as occurs in hyperparathyroidism, is associated with bone loss (particularly cortical bone), PTH can also exert anabolic effects on bone
• Unlike antiresorptive therapies that reduce bone resorption, parathyroid hormone (PTH) is an anabolic agent that enhances osteoblastic bone formation.
• Biologic activity of the intact hormone resides within the N-terminal 1-34 fragment; fragments from the mid- and C-terminal regions lack biologic activity.
• Teriparatide is a synthetic polypeptide hormone that contains the 1-34 amino acid fragment of recombinant human PTH (rhPTH [1-34]), a sequence identical to the biologically active N-terminal region of the 84-amino acid human PTH.
• They bind to specific cell-surface receptors on target cells in bone and kidney with high affinity.
• Daily single-dose administration causes a transient increase in serum PTH concentration, promoting new bone formation on both cancellous and cortical bone surfaces by preferential stimulation of osteoblastic activity over osteoclastic activity
• Continuous infusions, which result in a persistent elevation of PTH, lead to greater bone resorption than daily injections.
• Whereas daily injections of PTH increase bone volume, the net effect of continuous infusions is a decrease in bone volume.
• Daily PTH injections build bone by uncoupling bone turnover as the serum PTH level rises above normal for several hours, then falls below normal for many hours.
• The pattern of changes in serum PTH, combined with the pattern of elevation in biochemical markers of bone remodeling (increases in bone formation markers followed by increases in bone resorption markers), suggests a pathway through which daily PTH injection may temporarily uncouple bone turnover
• Teriparatide produces increases in bone mass and mediates architectural improvements in skeletal system
• These effects are lower when patients have been previously exposed to bisphosphonates, possibly in proportion to the potency of the antiresorptive effect

Dosage and uses:

• 20 microgm PTH exogenous PTH analogue (1-34hPTH; teriparatide) is used as a single daily SC injection for the treatment of postmenopausal osteoporosis in women with a high risk of fracture.
• These patients include women with a history of osteoporotic fracture, multiple risk factors for fracture, intolerance with osteoporosis therapy, or failure with therapy
• Teriparatide is also FDA-approved for the treatment of men with primary or secondary hypogonadal osteoporosis who are at high risk of fracture.
• After a 20-μg SC injection, PTH reaches peak serum concentration in approximately 30 minutes and declines to nondetectable levels within 3 hours.
• Combining PTH with antiresorptives has demonstrated even greater improvements in BMD that persist for at least 1 year after PTH is discontinued.

Adverse effects and Special Precautions:

• Side effects of teriparatide are generally mild and can include muscle pain, weakness, dizziness, headache, and nausea. Hypercalcemia can occur and symptoms typically appear 4 to 6 hours after injection
• Orthostatic hypotension can occur
• PTH should be used with caution in patients with urolithiasis and dose reduction is necessary in patients with renal insufficiency
• Teriparatide is not recommended for women who are pregnant or nursing.
• Teriparatide should not be prescribed for patients at increased risk for osteosarcomas, including patients with Paget’s disease of bone or unexplained elevations of alkaline phosphatase, children or young adults with open epiphyses, or patients who have undergone prior radiation therapy of the skeleton.
• In addition, teriparatide should not be administered to patients with preexisting hypercalcemia, bone metastases, or a history of skeletal malignancies or metabolic bone diseases other than osteoporosis

DEVELOPMENTAL COXA VARA

DEVELOPMENTAL COXA VARA
Aetiology:
primary defect in endochondral ossification of the medial part of the femoral neck.
Other theories regarding aetiology:
• Excessive intrauterine pressure on the developing fetal hip
• Vascular insult
• Faulty maturation of the cartilage and metaphyseal bone of the femoral neck

Bilateral in 30% to 50% of patients

Clinical Features:
• Present after they have started walking, but before 6 years of age.
• Painless limp due to a mild abductor weakness and mild limb length discrepancy
• If bilateral, the child presents with a waddling gait and increased lumbar lordosis
• The greater trochanter will be more prominent and proximal
• decreased ROM with maximum restriction in abduction and internal rotation.

X-Rays:
• Decreased femoral neck-shaft angle
• Vertical position of physeal plate
• Triangular metaphyseal fragment in inferior femoral neck with associated inverted Y appearance, which is pathognomonic.
• Shortened femoral neck
• Decrease in normal anteversion



Hilgenriener’s epiphyseal angle (H-E angle): Angle subtended by the horizontal line connecting the tri-radiate cartilage and the physeal line. Normal angle: <30°

Treatment
• HE Angle 45-60°: Observation and periodic follow up
• Indications for surgery: HE angle> 60°, progressive deformity, femoral neck shaft angle< 90°, development of trendelenburg gait
• Subtrochanteric valgus osteotomy. Adequate internal rotation of the distal fragment should be done to restore the femoral anteversion.
– Intertrochanteric osteotomy (Langenskold’s and Pauwel’s) is an alternative
– If the H-E angle is reduced to less than 38 degrees, 95% of the patients showed no evidence of recurrence
– Blade plate or a sliding hip screw is often used.
– An adductor tenotomy is frequently done.
– Spica cast immobilization is used, in addition, for 6 to 8 weeks in most patients.

Complications:
 Premature physeal closure may occur in the first 1-2 years after surgery.
 This can cause recurrence of the deformity
 Trochanteric apophysiodesis or a trochanteric advancement is done to prevent recurrence once physeal closure is documented.
 In case of recurrence of varus deformity a repeat valgus osteotomy is done