DNB December 2010 Theory papers

Paper 1
1. Define neuropathic joint. List the causes of neuropathic joint. Mention in brief the clinical features, diagnosis and treatment of neuropathic joint.
2. Define gout. Describe in brief its clinical features, diagnosis and treatment.?
3. Describe the broad principles of tendon transfer. Enumerate the tendon transfer for high radial nerve palsy.
4. Discuss the indications of surgery in TB spine with or without
neurological complications.
5. Draw a labeled diagram of brachial plexus. Classify brachial plexus
injury. Describe the clinical features and management of lower brachial
plexus injury.
6. Describe various types of lumbar root anomalies. List the
complications of lumbar disc surgery.
7. Define "Fat Embolism Syndrome". Describe in brief the clinical -
features, diagnosis and management of "Fat Embolism Syndrome".
8. Define Giant Cell Tumor (GCT) of bone. Describe in brief clinical
features, diagnosis and management principles of GCT of upper end
of tibia.
9. Describe aetiopathogenesis of avascular necrosis of hip. Classify
avascular necrosis of hip. Comment on broad principles of its
management.
10. Define ochronotic arthropathy. Describe its clinical features, diagnosis and management.

Paper 2


1. Define congenital muscular torticollis. List the differential diagnosis and outline the management of congenital muscular torticollis.
2. Describe the blood supply of scaphoid. Describe the clinical features, diagnosis and management of nonunion of scaphoid.
3. Define ulnar claw hand. Enumerate the causes of ulnar claw hand. Discuss its management.
4. Describe Dupuytren disease and its characteristic f,eatures. Describe in brief its pathogenesis prognosis and management.
5. Describe the hand deformities in rheumatoid arthritis. Describe in brief the Patho-anatomy and treatment of “Boutonneire deformity”.
6. Define pseudoarthrosis of tibia. Describe its pathogenesis, diagnosis, classification and management
7. Define Legg Calves Perthes disease. Describe its clinical features, diagnosis and management
8. Classify physeal injuries. Describe the management and complications of various types of physeal injuries.
9. List the causes of limp in a child.
10. Describe the Pathology and radiological signs in rickets and scurvy.

Paper 3
I. Classify proximal humerus fracture. Discuss the management options for various types. Outline the management for type IV fracture in elderly females.
2. Describe pitfalls in using the Locking Compression Plate.
3. Classify open fractures of tibia. Describe the management of type 3 b open fracture of tibia.
4. Describe briefly the etiology, clinical features, diagnosis, investigations and treatment of painful elbow following injury around elbow.
5. Describe classification of Monteggia fracture dislocation and its management.
6. Define nonunion. Describe the classification and broad principles of management of diaphyseal nonunion.
7. Define Tension Band principle. Describe the use of Tension Band principle in fracture surgery.
8. Define external fixation. Classify the external fixators. Describe the advantages and disadvantages of external fixation.
9. Classify thoracolumbar spine injuries. Give radiological classification of burst fracture. Outline the management of burst fracture of LI vertebra.
10. Describe various methods of treatment of distal radius fracture with their principles.


Paper 4
1. Describe different types of bone grafts along with their properties.
2. Describe the phases of normal gait and the types of muscle contractions in gait cycle.
3. Write short note on Nuclear medicine and its applications in Orthopedics.
4. What is flap reconstruction? Write its classification.
5. What are the types of epiphysis? Describe the types, various methods and indications of epiphysiodesis.
6. Write short note on Coxa Vara.
7. Describe pathogenesis of acute compartment syndrome and its diagnosis.
8. Name biomaterials used in orthopedics. Describe in brief their features.
9. Describe nerve injuries, Sunderland Classification, outcome expected and basis of repair.
10. Describe the various foot and ankle deformities in cerebral palsy and their management.

Book Released

Dear friends,

Finally the book has arrived. Orthopaedic Principles-A Review is ready for you. I am here by attaching the cover page. The foreword has been written by Dr Ashok Johari, President of Indian Orthopaedic Association and Editor-in-chief of Journal of Paediatric Orthopaedics (B).

- The book will run into 750 pages and will comprise 110 diagrams that are essential for understanding a specific pathology/technique.
- The book is largely based on the Instructional Course Lectures (ICL) of JBJS, JAAOS. DNB theory questions are often based on a recent ICL.
- The book tries to solve past 10 years DNB questions.
- The chapters are arranged according to speciality(eg, sports medicine, joint reconstruction etc)
- The format is bullet format(similar to Handbook of Fractures by Kenneth Koval)
- Important references have been included that will help you go through original articles
- MCQs have been placed in such a way, so that you reinforce your knowledge by applying it to clinical conditions.


Warm Regards and best Wishes,
Dr Hitesh Gopalan U
Editor-in Chief, Orthopaedic Principles
Co-ordinator, Indian Orthopaedic Trainees Association (InOTA), affiliated to IOA.

For Book Orders:
Email: arthritis.research.kochi@gmail.com
Telephone: 9747093443

Anterior Shoulder Instability

Definition
• Stabilizing Factors
• Tests - LAXITY TESTS, INSTABILITY TESTS
• Imaging – Radiographs, CT, MRI, MR arthrography
• Classification, Matsen’s TUBS & AMBRII
• Surgical options: Anatomic Reconstruction (Bankart Repair and Montgomery and Jobe modification);
• Non-Anatomic Reconstruction (Bristow Latarjet Procedure, Putti- Platt Procedure, Magnuson Stack Procedure, Neer’s, O’Brien)
• Current Recommendations
• Clinical Scenarios

Definition of Shoulder Instability:- Abnormal symptomatic motion of the humeral head relative to the glenoid during active shoulder motion.


Stabilizing Factors:
• The mechanisms providing stability can be categorized as ‘static’ and ‘dynamic’.
• The rotator cuff muscles form the ‘dynamic’ stabilizers whereas the articular anatomy and the capsuloligamentous complex form the ‘static’ stabilizers.
• In all, the glenohumeral joint is stabilized by following key elements:
1. Concavity of the glenoid
2. The muscles that compress the humeral head into the glenoid.
3. The coracoacromial arch
4. The capsuloligamentous restraints
5. Adhesion-cohesion of the articular surfaces
• The above mentioned elements function inter-dependently to keep the humeral head stable in the glenoid cup. Deficiencies or defects in any of these structures or incoordination between the structures can lead to instability.

Factors influencing probability of recurrent dislocation:
1. Age,
2. return to contact/collision sports,
3. bony defect (glenoid /humeral head)
Glenoid Concavity
The glenoid concavity is formed by three components:
1. the osseous glenoid - slightly concave
2. the articular cartilage - thicker at the periphery and thinner in the center making the concavity deeper and
3. the glenoid labrum - further deepens the glenoid concavity by 50%
• The concavity of the glenoid provides stability to the humeral head similar to a ball which sits at the centre of a concave surface.
• The adequacy of the glenoid concavity in different directions can be assessed clinically by the ‘load-and-shift test’.


Muscles that compress the humeral head
• The humeral head is compressed into the glenoid by the muscles of the rotator cuff and other scapulohumeral and thoracohumeral muscles.
Subscapularis - primary anterior compressor
Supraspinatus - primary superior compressor
Infraspinatus – primary posterior compressor (assisted by teres minor)
• The rotator cuff muscles function as head compressors in almost any position of the glenohumeral joint, except the terminal range.
• Other muscles, such as deltoid, long head of the biceps, pectoralis, latissimus, teres major and pectoralis major contribute to humeroglenoid compression in certain other positions. For example, deltoid becomes a strong compressor of the head into the glenoid when the arm is abducted 90°.
• Paralysis, detachment, or dysfunction of any of the rotator cuff muscles results in loss of humeral head compression.


The Glenohumeral Ligaments and Capsule
• During rotation of the arm, the glenohumeral ligaments and capsule tighten and loosen reciprocally, thus limiting translations and rotations in a load-sharing fashion.
• The glenohumeral capsule and its associated ligaments are lax and do not exert a centering effect in mid-range positions (Compare muscular stabilizers). However at the extremes of motion, these structures become important contributors to humeral centering. They prevent humeral rotation beyond the point where the muscles are effective.

Adhesion-Cohesion
• The surfaces of the humeral and glenoid cartilage and the surfaces of the coracoacromial arch and the proximal humeral convexity adhere to each other because of the adhesive and cohesive properties of water molecules giving a smooth glide for the surfaces while simultaneously preventing them from separating.

The Suction Cup Mechanism
• The negative intra-articular pressure in the joint makes the pliable labrum centered by a non-compliant osseous glenoid stick to the humeral head like a suction cup.
• Both the adhesion-cohesion and the suction-cup mechanism are non-energy- consuming.
• Conditions where these mechanisms are lost: 1) fracture of the glenoid lip, 2) when the joint surfaces are not covered with smooth wettable hyaline cartilage eg. Glenohumeral arthritis or following total shoulder replacement, 3) both are also lost when there is joint effusion or hemarthrosis.

Evaluation of Glenohumeral Instability:
Patient History
• Age of 1st dislocation event or instability- Younger the age, higher is the chance of recurrent instability. <20yrs->40yrs 10%,but more tendency to fracture with dislocation
• Onset- Traumatic or Atraumatic
o History of trauma?
o Frank dislocation that required manual reduction or a subjective feeling of instability of the shoulder (subluxation)?
• Position of the arm at the time of instability- To know if the dislocation was anterior or posterior
• Any particular position or movement exaggerating the pain or produces sense of instability?
• The number of discrete instability events and the degree of disability?
• The ability to voluntarily dislocate the joint? Surgical management of instability in this patient population may result in high rates of recurrence.

Physical examination
Physical examination for shoulder instability can be divided into two main groups:
(1) tests for glenohumeral laxity and
(2) tests for glenohumeral instability.
(3) tests for generalized ligamentous laxity

Laxity Tests:
Anterior Drawer Test
• Quantifies the amount of anterior translation.
• Patient lying supine, examiner stands at the ipsilateral side of the affected extremity. The patient’s hand is positioned in the examiner’s axilla. The shoulder is in 80o to 120o of abduction, 0o to 20o of forward flexion, and 0o to 30o of external rotation. The scapula is stabilized with one hand. The other hand grasps the proximal humeral shaft and exerts an anterior force. The amount of translation is quantified.
Posterior Drawer
• Patient in supine position. For left shoulder, the patient’s left wrist and forearm is held with the elbow flexed to 120o. With the shoulder in 80o to 120o of abduction and 60o to 80o of forward flexion and internal rotation, a posterior force is applied on the arm. The amount of posterior translation is assessed by the hand stabilizing the scapula.
Lachman test
Patient supine, extremity in various degrees of abduction and external rotation in the plane of the scapula. Anterior stress is applied to proximal humerus. The amount of translation and the end point are evaluated.
Anterior and Posterior Load and Shift Test
• Supine position with arm in 20o of abduction, 20o of forward flexion and neutral rotation or upright position with arm by the side of torso.
• The examiner grasps upper arm and applies an axial load perpendicular to the articular surface of the glenoid. Anterior or posterior-directed forces are then applied the humeral head and translation relative to the glenoid is measured.
Gage Hyperabduction Test
• It is a measure of laxity of the inferior glenohumeral ligament complex.
• The test is performed with the patient sitting and the examiner standing behind. With one hand stabilizing the scapula, the other hand is used to abduct the affected shoulder.
• The amount of abduction measured before the initiation of scapula motion is recorded.
• The amount of abduction where glenohumeral motion ends and scapulothoracic motion begins is the passive motion of the shoulder in abduction.
• A value greater than 105o is suggestive of inferior glenohumeral ligament laxity.
Sulcus Sign
• It is positive when there is increased inferior translation of the humeral head relative to the glenoid with applied downward traction in patients with inferior and multidirectional instability.
• The sulcus should be measured at both neutral and 30o of external rotation. Elimination of the sulcus sign with external rotation suggests competency of the rotator interval; persistence of sulcus sign at 30o of external rotation suggests a lax rotator interval.

Grading of Humeral Translation
• grade 0 - Minimal inferior translation
• grade I – 0 to 1 cm translation (or) greater than the opposite uninvolved extremity
• grade II - 1 to 2 cm translation (or) humeral head translation to the glenoid rim
• grade III - greater than 2.0 cm translation (or) translation over the glenoid rim
• grade IV - indicates dislocation during testing

Instability Tests:
Apprehension Test• Patient in supine or upright position.
Anterior apprehension test:
• Affected shoulder is passively moved to abduction and maximum external rotation and a gentle anterior force is placed on the posterior humeral head. Test is positive when the patient becomes apprehensive and experiences pain.
Posterior apprehension test
• The affected shoulder is adducted and internally rotated.
Apprehension-Relocation Test:
• After apprehension test, a posterior-directed force is applied to the anterior humeral head. There is relief of apprehension. This is also called “Fowler’s sign”.

Anterior Release and Surprise Test
• The patient is in the supine position. The affected shoulder is held over the edge of the examiner’s table. The arm is positioned in 90o of abduction. A posterior directed force is applied to the anterior humeral head while simultaneously moving the shoulder to maximum external rotation. The posterior force is then released.
• The test is positive when the patient experiences pain and apprehension.

Imaging:
Radiographs:
Basic Views
• True anteroposterior (AP) view of the G-H joint
• Supraspinatous Outlet View (SSOV) also called lateral or Y view in the scapular plane and an Axillary view
Special Views
Stryker-notch view:
• For Hillsach’s Lesion
• Patient lying supine with the cassette placed posterior to the shoulder. The hand of the affected extremity is placed on top of the head with the elbow pointing straight upward. The radiograph beam is directed 10o cephalad and centered over the coracoid process.
West Point axillary view:
• For Bony Bankart or Glenoid fracture.
• Patient lying prone with the affected shoulder resting on a pad. The radiograph beam is aimed 25o from the horizontal plane (angled toward the table surface) and 25o toward the patient’s midline.

CT scan
• Useful for assessing bone defects on humeral or glenoid side.
• CT scan should be considered if patient reports instability at low abduction angles or has marked apprehension at low abduction/external rotation during provocative testing
• To determine the percentage of defect, the area of bone loss is divided by the area of a circle based on the inferior glenoid and the quotient is multiplied by 100%

MRI and MR arthrography
• Gold standard for evaluating the capsulolabral structures especially the Bankart’s lesion (Detachment of anterioinferior glenoid labrum and the inferior gleno-humeral ligament from the glenoid).
• The addition of contrast can improve the ability of MRI to show rotator cuff pathology, humeral avulsion of glenohumeral ligament(HAGL), capsular tears
Examination under anesthesia confirms laxity but not instability.
Arthroscopy is an excellent technique for confirming shoulder instability.

Classification:
Shoulder instability can be classified based on the direction, degree, and duration of symptoms and direction of instability should be categorized as unidirectional, bidirectional, or multidirectional.
Matsen’s Classification
TUBS: Traumatic, Unidirectional , with a Bankart’s lesion, requires Surgery and
AMBRII: Atraumatic, Multidirectional and Bilateral, responds to Rehabilitation, occasionally requires an Inferior capsular shift and Internal closure.
Surgical options:
Checklist for treating Shoulder Instability
1. Unidirectional/ Multidirectional.
2. Status of Dynamic stabilizers (Rotator cuff and Long head of Biceps).
3. Status of Capsuloligamentous structures (Glenohumeral ligaments/ Capsule).
4. Status of articulating bones (Humeral head defect/ Glenoid bone deficiency).

Anatomic Reconstruction
Bankart Repair

Principle: Reattachment of the antero-inferior glenoid labrum and the IGHL back to the glenoid anatomically.
Procedure: Open/ Arthroscopic
Subscapularis and anterior capsule are opened vertically. Lateral leaf of capsule is attached to anterior glenoid rim. Medial leaf is imbricated and subscapularis is approximated.
Adv: Corrects labral defect, no metallic internal fixation device required.
Disadv: Technical difficulty, restriction of external rotation.
Modified Bankart repair: Modified by Montgomery and Jobe. Anterior capsule imbricated in north-south direction. Hence external rotation not lost.

Keys to success of Bankart surgery
1. Abrading the scapular neck
2. Restoring glenoid concavity
3. Anatomical capsular fixation at the edge of glenoid
4. Superior and inferior capsular advancement and imbrication
5. Goal oriented rehabilitation

Non-Anatomic Reconstruction
• Bristow Latarjet Procedure- Transfer of coracoid to anterior glenoid rim
• Putti- Platt Procedure- Reefing the subscapularis and anterior capsule of the shoulder joint.
• Magnuson Stack Procedure- Lateral transfer of the subscapularis tendon attachment.
• Inferior Capsular Shift (Neer’s procedure)- Described for Multidirectional instability to reduce the volume of the joint. T shaped incision starting from the glenoid neck. Obliterates the capsular redundancy on the side of surgery and also on the opposite side.
• O’Brien modification of Neer procedure: Capsular shift procedure with the T portion of the incision starting adjacent to the glenoid. Allows much easier repair of a detached glenoid labrum if present.
- Weber osteotomy: Subcapital rotational osteotomy of proximal humerus for large humeral defects. The procedure rotates the defect to a more posterolateral position to avoid levering of the humeral head on the glenoid at the Hill-Sachs lesion.

• Anterior instability without bony defect - Anatomic reconstruction (Bankart repair)
• Anterior instability with humeral head defect of
<20% - Reduction + Immobilisation/ Bankart anterior stabilisation
20-30%: Acute-Disimpaction; Old-Bankart repair
30-45% - As above/ Bone graft/ Weber osteotomy
>45% - Prosthetic replacement
• Anterior instability with anteroinferior glenoid defect of
<20% - Bankart repair
>20% - Bone graft/ Corocoid transfer



•

Foreword for Orthopaedic Principles-A Review

FOREWORD

The Indian Orthopaedic Trainees just like trainees elsewhere, need strong foundations in Orthopaedics and Traumatology. When it comes to examinations, however, they need a book which summarises the highlights of an orthopaedic topic. They should be able to go through it quickly and it should present important and factually correct information. In a sense, this is a different recipe for gathering knowledge for ready reference. ‘Orthopaedic Principles’ fulfils such a requirement and as such can be highly recommended for trainees who desire rapid education.

With the coming into being of the Indian Orthopaedic Trainees Association (IOTA), a new forum has come wherein feedback from the trainees is respected and where the trainees work to benefit their community. This is of course with the backing and support of their trainers and of the Indian Orthopaedic Association. The Indian Orthopaedic Trainee while respectful of his trainers, is maturing into an individual who can question, analyse and beg to differ. It is in this climate and culture that this book is born and I hope that the Indian Orthopaedic Trainees Association adopts it as a standard text for trainees.

Dr. Hitesh Gopalan and his team are a bunch of young energetic orthopaedic surgeons who understand the needs and aspiration of trainees and have tried to fulfil them. Dr. Gopalan is the inland coordinator for IOTA and runs a wonderful website on Orthopaedic Principles. I hope his team continues its good work to bring Indian orthopaedic training as a model on the world stage.


Prof. Dr. Ashok N. Johari
M.S. Orth., M.Ch.Orth (Liv), D.N.B. Orth., D.Ortho.,
F.C.P.S., F.R.C.S. (Lon), F.A.M.S.
President, Indian Orthopaedic Association
President, Paediatric Orthopaedic Society of India
President, Indian Academy of Cerebral Palsy
Editor in chief, Journal of Pediatric Orthopaedics (B)
Hon. Fellow, British Orthopaedic Association

Formation of Indian Orthopaedic Trainees Association

Message from Dr Ashok Johari,
President,
Indian Orthopaedic Association

IOA President's Theme initiative on ‘Better Patient Care …. Through Education and Research’

INDIAN ORTHOPAEDIC TRAINEES ASSOCIATION (IOTA), affiliated to Indian Orthopaedic Association

On a proposal by the President, IOA, the executive committee at its meeting in May, 2010, passed the creation of an Indian Orthopaedic Trainees Association (IOTA). This will be supported by the IOA as an important affiliate. The idea of having a body like this is as follows:

1. All orthopaedic trainees can come together to discuss and find solutions to the problems relating to their training. They can contribute their view point and become an important voice in shaping policies relating to training and other issues which concern them.
2. To help orthopaedic postgraduates in India obtain the highest levels of orthopaedic knowledge by organizing their own CME and other training programs.
3. Establishing and availing awards and training fellowships
All postgraduates, trainees, residents and fellows can join this organization by becoming associate life members of the IOA. They will progress to full life membership of IOA once they fulfill all eligibility criteria for such membership.

Activities possible under the banner of IOTA
· To prepare an orthopaedic trainee throughout his course on how to go about his course.
· To ensure all orthopaedic postgraduates get access to peer reviewed journals and instructional course lectures
· To initiate webcasting of “clinical examination” as performed by the best clinicians to all postgraduates in India
· To inculcate in young minds the importance of research and guide them on ‘proper research methodology’
· To organize videos of ‘important’ orthopaedic operations performed by the expert, that will help the postgraduate learn before he attends a particular operation during his training
· To prepare Course Lectures (in par with AAOS/OKO) and give access to all postgraduates
· By conducting a 2 day crash course lecture series (comprising 50-100 topics) to help DNB students pass their theory exam, which will be conducted once or twice a year(in lines with FRCS Tr and Orth training)
· If possible to begin a practical exam training course, conducted every year, either undertaken solely by IOTA or in association with existing courses (e.g. Calicut course, Indore Course, MAMC Course, Hyderabad course, St John’s Course)
· To inculcate in young minds the importance of subspeciality training and encourage them to pursue fellowships in India as well as abroad
· To ensure all orthopaedic trainees in India get to know about their regional as well as national level CME’s through a comprehensive website.
· To contact all postgraduate institutions and discuss with their teachers that such a body exists and to utilize the best resources
· To bring out a complete manual for orthopaedic postgraduates, which will cover all aspects of their training.
· To have a post graduate teaching session and other sessions during the IOACON and IOAICL.

Organisational Structure
The first meeting of IOTA will take place during the IOACON, 2010, at Jaipur. Prior to this, information relating to the formation of IOTA would be circulated to all institutions and teaching centres through this newsletter and through the IOA and other websites. All trainees keen to join IOTA would become Associate Life Members of IOA by proper application to the IOA Headquarters at Delhi. They should contact Mr. Ramesh Panday, the Executive Officer of IOA, on his e-mail id. ioahouse_org@yahoo.com / rc_panday@yahoo.com. An adhoc committee would be formed by those present with the following composition:
Board of Directors (Six, to include the current President of IOA, its Secretary, Treasurer, 2 Past Presidents and the President Elect))
- IOTA President (One)
- Vice President (One)
- Secretary (One)
- Executive Committee Members (Four)
- Coordinator (One)

This committee would design the Constitution of IOTA to include the mode of election, term of office, responsibilities etc. The initial funding for running of IOTA and its programmes would be borne by the IOA as a joint IOA-IOTA exercise. In later years it is envisaged that IOTA would become self sufficient through grants and donations to be able to meet its own expenses. At this point in time, the Board of Directors would be reduced to Five to exclude the Treasurer of IOA and a separate post of treasurer would be created in the IOTA executive.
Views of members of IOA, institutions concerned with training of orthopaedic trainees and those of the trainees themselves are invited. Please send your views latest by 15th of August on e-mail to Dr. Ashok Johari at drashokjohariAThotmailDOTcom labeled IOTA. The first coordinator for IOTA is Dr. Hitesh Gopalan who is contactable at hitheshgATyahooDOTcom.

Experiences of Senior Orthopaedic Surgeons

Hot Discussion in our forum:

Forum Updates:

Experts talk about their life as an Orthopaedic Surgeon:

Posts by Dr Rajesh Purushothaman, Associate Prof, Calicut Medical College,
Dr MC John, former Consultant Medical Trust hospital.

Dr Ayappan Nair, senior consultant joins forum.

Dr Shishir Rastogi(AIIMS), Dr NK Pradhan comments @ guestbook

visit:

http://orthopaedicprinciples.com/forums/viewtopic.php?f=9&t=25

Orthopaedic Principles Website

Hi everyone,

We hereby take pleasure in announcing the launch of our website,

www.orthopaedicprinciples.com

to look into the needs of Postgraduates and young orthopaedic surgeons. We are embarking on an “active discussion forum”, which is an extension of the highly successful communities that we run in orkut and facebook, with more than 700 postgraduate members altogether.

The topics discussed are shown in the following image. So join the forum and start posting.



A larger part of the website in under construction.

Regards,

Editorial Board
Orthopaedic Principles

SCHEUERMANN's DISEASE

SCHEUERMANN DISEASE

Hitesh Gopalan U, MS, Senthilnathan MS MD.

Theories of Origin
 Scheuermann proposed that the kyphosis resulted from avascular necrosis of the ring apophysis of the vertebral body.
 Schmorl suggested that the vertebral wedging was caused by herniation of disc material into the vertebral body.
 Ferguson implicated the persistence of anterior vascular grooves in the vertebral bodies, which create a point of structural weakness in the vertebral body, which leads to wedging and kyphosis.
 Bradford et al suggested that osteoporosis may be responsible for the development of Scheuermann disease.
 Mechanical factors: Common in patients who do heavy lifting or manual labour.
 Ippolito and Ponseti suggested that a biochemical abnormality of the collagen and matrix of the vertebral endplate cartilage.

Criteria for Diagnosis (Sorenson criteria)
• More than 5 degrees of anterior wedging of at least three consecutive vertebrae at the apex of the kyphosis and vertebral endplate irregularities.
• Thoracic kyphosis of more than 45 degrees.


Natural history of the disease:

• Adult patients with mild deformity( Mean 71 degrees) present with chronic back pain.
• More severe defomities cause severe chronic back pain.
• Pulmonary compromise generally occurs if the curve is more than 100 degrees.
• Patients with type II Scheuermann's kyphosis almost never require surgery

Classification
– There are two forms of Scheuermann's kyphosis—type I and type II.
– The classic thoracic type (type I) has an apex between T7 and T9 and is associated with increased lumbar lordosis.
Type I (typical) again divided into 2 types
 Type a(thoracic) extends from T1-2 to T12-L1 and apex at T6-T8 and
 type b(thoracolumbar) extends from T4-5 to L2-3 and has apex at
Thoracolumbar junction.

– The thoracolumbar or lumbar type (type II) has a lower apex, which frequently is associated with reduced upper thoracic kyphosis or thoracic lordosis.
– Type II Scheuermann's kyphosis occurs more frequently in males in a slightly older age group (15 to 18 years).
– This form tends to be more painful but rarely leads to progressive deformity

Clinical Features:

* In Scheuermann’s disease the deformity does not disappear on lying supine or with hyperextension manouevre.
* Pain is usually at the apex of the deformity
* Kyphosis is often rigid and cannot be corrected by hyper extension
* Neurological examination is often normal, because kyphosis occurs gradually and over several segments
* The onset is often after lifting heavy weight from a flexed position.
* Lumbar Scheuermann is less common and the deformity is often minimal.
* Rarely, thoracic disc herniation, epidural cysts, or a severe kyphosis (>100 degrees) can cause neurologic deficit in patients (usually adults) with Scheuermann's kyphosis

Imaging:

• lateral x-rays: to measure vertebral wedging and measure Cobb’s angle of deformity
• May also reveal vertebral end plate irregularities, narrow disc spaces and Schmorl’s nodes
• In 20% to 30% of patients, the posteroanterior x-ray shows associated mild scoliosis in the area of the kyphosis.
• The scoliotic apex usually corresponds with the kyphotic apex.
• A lateral x-ray should be examined for spondylolisthesis in addition to kyphosis.
• In the later stages of Scheuermann's kyphosis, x-rays may show changes of degenerative arthritis, including decreased intervertebral disc spaces, marginal osteophytes, and ankylosis
• MRI: to rule out disc herniation if patient is planned for posterior surgery

Differential Diagnosis:
1. Postural kyphosis:
– In a forward bending test, the kyphotic deformity is accentuated, and the apex appears as a sharp angulation, in contrast to the smooth curve of a patient with postural kyphosis.
– A forward bending test also exposes any associated scoliosis.
– The hyperextension test helps the examiner understand the rigidity of the curve.
– A curve that is flexible or reduces significantly with hyperextension is typically postural and not Scheuermann's kyphosis, although in younger children a flexible round-back deformity may be the first sign of evolution to true Scheuermann's kyphosis.

Treatment:

Conservative:

• Bracing - effective in controlling the progression of deformity.
 Indicated in patients with kyphosis less than 1year of onset, curves between 50-70 degrees and apex below T7.
 Bracing is continued for at least 18 months.
 Acute application of a brace can influence the deformity and improve kyphosis by 40% to 50%; however, several articles have shown at least partial loss of this correction when brace wear is stopped.
 All kyphosis braces require careful orthotist attention to ensure fit and to recontour the posterior bars and pads every 2 months to gain further correction progressively.

• Pain usually responds to NSAID's and physical therapy.

• Surgical:
 Posterior correction with or without osteotomy and fusion.
 Anterior release has been recommended for deformities that do not correct to 50 degrees on stress views.
 Fusion level: Current recommendations are to include the proximal end vertebra (determined by the modified Cobb method) and to extend the fusion past the transitional zone to the first lordotic disc distally
 Traditional teaching is to restrict the correction to 40 degrees to prevent proximal or distal junctional kyphosis and implant pull out.
 Intraoperative neurologic monitoring is crucial during any surgery to correct kyphosis because the thoracic cord is at risk during correction and instrumentation. NMEPs and SSEPs are used for this.
 postoperative bracing for approximately 3 to 6 months

• Relative indications for surgery:
Kyphosis more than 70 deg, Deformity progression despite bracing, cosmesis, neurologic
deficits and failure of conservative treatment for pain.

Contraindications: Asymptomatic patient without cosmetic concerns.

Ref:
1. Papagelopoulos PJ, Klassen RA, Peterson HA, et al. Surgical treatment of Scheuermann's disease with segmental compression instrumentation. Clin Orthop 2001;386:139-149.
2. Otsuka NY, Hall JE, Mah JY. Posterior fusion for Scheuermann's kyphosis. Clin Orthop 1990;251:134-139.
3. Tribus CB. Scheuermann's kyphosis in adolescents and adults: diagnosis and management. J Am Acad Orthop Surg 1998;6:36-43.
4. Wenger DR, Frick SL. Scheuermann kyphosis. Spine 1999;24: 2630-2639.

Intercondylar Fractures of the Elbow

INTERCONDYLAR FRACTURES

Mechanism of injury:
Is by a force directed towards an elbow which is flexed > 90° which causes the ulna to drive against the trochlea

Riseborough and Radin Classification
• Type I: Nondisplaced
• Type II: Slight displacement with no rotation between the condylar fragment.
• Type III: Displacement with rotation
• Type IV: Severe comminution of the articular surface.

Classification of Mehne and Matta:
1. High T.
2. Low T
3. Y-type
4. H-type.
5. Medial.
6. Lateral

The Mehne and Matta classification describes the most often encountered fracture patterns intraoperatively.

Clinical Features:
1. The elbow maybe held in 90° flexion and forearm is kept pronated
2. Crepitus may be elicited
3. Independent mobility of the medial and lateral condyle can be elicited
4. The normal 3 point bony relationship between the olecranon, medial epicondyle and lateral epicondyle is lost

X-Rays:
Standard AP and lateral views are obtained
CT scan is helpful to further delineate the fracture pattern

Nonoperative Treatment
• Elderly patients with severe osteopenia and comminution or Patients with significant comorbid conditions precluding operative management.

Operative Treatment

Open reduction and internal fixation:
• Restores articular congruity
• Interfragmentary screws and dual-plate fixation: One plate is placed medially and another plate posterolaterally. Reconstruction plate and one-third plate are used commonly.
• Total elbow arthroplasty (semi constrained): May be considered in markedly comminuted fractures and in fractures with osteoporotic bone.

Pearls of Internal fixation for distal humerus fractures (O’Driscoll et al..)

1. olecranon osteotomy provides the best exposure of the articular surface of the distal humerus (1), but problems due to non union and symptomatic implants maybe seen
2. Alternative approaches include the triceps reflecting, anconeus pedicle, or TRAP exposure described by O'Driscoll or elevating the triceps from the posterior humerus, but leaving it attached to the olecranon(Allonso Llamas) approach(2)
3. Identify the ulnar nerve and protect it throughout the procedure.
4. Transpose the ulnar nerve if hardware is placed medially to prevent irritation from the hardware
5. Perform the olecranon osteotomy in the area of the olecranon that is normally devoid of articular cartilage.
6. Drill and tap olecranon prior to performing the osteotomy.
7. When performing the olecranon osteotomy, remember that the semilunar notch is “V-shaped” with the central area being the thickest (the site for the osteotomy—about 2 cm distal to the olecranon tip)
8. Create a chevron osteotomy with the apex pointing distally.
9. Anatomic reduction and preliminary fixation with Kirschner wires or interfragmentary lag screw fixation of the articular condyles
10. Fixation of the lateral column with a well-molded posterior plate
11. Fixation of the medial column with a medial plate extending down to, and on occasion wrapping around, the medial epicondyle
12. Multiple interfragmentary screws, usually through the plates or independent of the plates, to secure the fracture construct together
13. If one large fragment of the joint surface can be reduced to either medial or lateral column, it can be used to surgeon’s advantage. Once this stable construct has been established other fragments can be added
14. Try to place every screw in a fragment through the plate
15. If the fracture extends distally, the plates should be contoured over the respective epicondyles and placed adjacent to the articular margin
16. Distal plate placement may result in impingement during terminal elbow extension
therefore, before definitive plate fixation the elbow should be examined to ensure an acceptable ROM with absent bony or soft tissue impingement
17. Some surgeons prefer cannulated screws because these can be placed over the preliminary K- wires
18. Avoid injury to the radial nerve by identifying the nerve if proximal exposure is necessary.
19. Avoid narrowing the trochlea with lag fixation in cases with articular comminution.

Ref:
1. Wilkinson JM, Stanley D. Posterior surgical approaches to the elbow: a comparative anatomic study. J Should Elbow Surg 2001;10:380-382.
2. Alonso-Llames M. Bilaterotricipital approach to the elbow. Acta Orthop Scand 1972;43:479-490.
3. Muller ME, Allgower M, Schneider R, et al. Manual of internal fixation. Techniques recommended by the AO-ASIF Group. 3rd ed. Berlin: Springer-Verlag; 1991.
4. O’Driscoll SW, Jupiter JB, Cohen MS, Ring D, McKee MD: Difficult elbow
fractures: Pearls and pitfalls. Instr Course Lect 2003;52:113-134.

Os Trigonum Syndrome

• Is a cause of posterior ankle pain.
• The lateral (posterior) tubercle of the talus has a separate center of ossification, which appears from ages 7 to 13 years.
• When this fails to fuse with the body of the talus, it is called os trigonum
• It lies lateral to the groove for the flexor hallucis longus (FHL) tendon
• A cartilage connection may or may not attach the os trigonum to the talus.
• The os trigonum has been reported to be present in 1.7% to 7% of normal, asymptomatic feet

Clinical features:
• gradual onset of pain, especially in the anterior aspect of the retrocalcaneal space
• Pain is recreated by forced plantar flexion of the ankle
• pain may be elicited by direct pressure over the posterior lip of the talus

Imaging:
• May be visible on plain radiographs.
• Stress views with the ankle in plantar flexion can show the posterior impingement.
• Three-phase bone scanning may show increased radioactivity in the case of a symptomatic nonunion.
• However, not all os trigonum with positive bone scans are symptomatic.
• CT scan: can provide detailed visualization, especially of a fibrous union or nonunion.
• MRI: may show edema within the os trigonum fragment, as well as fluid around it.

Treatment:
• Nonoperative treatment consists of NSAIDs, activity modification, and occasionally immobilization.
• Surgical treatment may be indicated if nonsurgical management fails.
• Excision can be performed arthroscopically.
• The os trigonum is visualized through the anterolateral portal, and working portal is the posterolateral portal.
• Excision is performed using arthroscopic banana knives, curettes, and graspers.
• Care should be taken to avoid injury to the FHL tendon and the posteromedial neurovascular structures.
• Cure rates with surgery are high

ACROMIOCLAVICULAR JOINT INJURIES

ACROMIOCLAVICULAR JOINT INJURIES

Mechanism of Injury:
1. Direct force is the commonest cause due to fall on the shoulder with arm adducted
2. It can also occur with indirect force due to fall on the outstretched hand

Features of Acromioclavicular joint:
• Is a diarthrodal (synovial) joint
• Horizontal stability is provided by the acromioclavicular ligaments
• The AC joint has a thin capsule that is stabilized by anterior, posterior, superior, and inferior AC ligaments. Superior AC ligament is the most important of all ligaments
• A fibrocartilaginous disk of varying size and shape exists inside the joint
• Vertical stability is by the coracoclavicular ligaments
• Normal coracoclavicular distance is 1.1 to 1.3 cm

Rockwood Classification
• Type I: Sprain of the AC ligament
Normal radiograph
• Type II: AC ligament tear, coracoclavicular ligaments sprained
Radiograph demonstrates AC joint widening (normal AC joint distance is 1 to 3mm). Stress views show identical coracoclavicular distance compared to uninvolved side
• Type III: AC and coracoclavicular ligament torn.
Radiograph demonstrates loss of AC joint relationship and increased coracoclavicular distance in stress view (25% to 100% greater than the normal side.).
• Type IV: Type III with distal clavicle displaced posteriorly into or through the trapezius
• Type V: Type III with the distal clavicle grossly displaced superiorly.
• Type VI: AC dislocated with the clavicle displaced inferior to the acromion or the coracoid.

Clinical Features:
• As in all fractures pain, tenderness and difficulty in moving the affected part is seen.
• An apparent step-off deformity is seen at the AC joint
• There may tenting of the skin over the distal clavicle

X Rays:
• AP view of the shoulder, scapular Y view and axillary views
• Zanca view: A 15 degree upward tilt view best visualizes the AC joint
• Stress views of the AC joint are obtained by tying 10 to 15 lb weight to the wrists and taking an AP view. The Acromioclavicular and coracoclavicular distances are compared with the normal shoulder.
• Stryker notch view: will rule out an associated coracoid fracture. A coracoid fracture is suspected when there is an AC joint dislocation on the AP projection but the coracoclavicular distance is normal, or equal to that on the opposite, uninvolved side

Treatment
• Type I: Sling immobilisation
• Type II: Sling immobilisation
• Type III: Inactive, non-labouring patient: -nonoperative treatment with sling. Operative treatment in heavy labourers.

• Type IV, V, VI: Open reduction and surgical repair of coracoclavicular ligaments.

• When surgical repair is done, open reduction is performed and acromioclavicular joint is fixed with K wires or indirect fixation is achieved by coracoclavicular fixation with a Bosworth screw.
• Reconstruction of the coracoclavicular ligaments is performed by using the coracoacromial ligament as a substitute, and by the placement of a synthetic augmentation device (such as a band made of absorbable braid or ribbon, Dacron tape) between the coracoid and clavicle

Clavicular HOOK PLATE:
• The clavicular hook plate was developed for treatment of AC joint dislocations and claviCLe fractures in which the distal fragment is too small to allow conventional plate fixation .
• The plate has an offset lateral hook, designed to engage distal to the posterior aspect of the acromion.
• It has been used with some success for displaced lateral-end clavicular fractures, but there are concerns that the plate may induce shoulder stiffness and osteoarthritis of the acromioclavicular joint, and there is also a risk of skin slough and infection.
• Improper positioning of the hook may lead to inadequate fixation.
• Osteolysis has been noted around the hole for the hook as shoulder movement increases, and most surgeons advise routine plate removal at three months after implantation, which necessitates a second operation.
• The timing of plate removal is critical, as early removal may result in nonunion or refracture due to instability at the fracture site, whereas delayed removal can lead to shoulder stiffness or even fracture medial to the plate


Advantages and disadvantages of AC joint dislocation fixation methods:
a)Intra-articular AC fixation
Adv: Anatomic reduction
Disadv: Hardware failure or migration
Distal clavicle osteolysis

b)Extra-articular coracoclavicular repairs
Adv: Superior strength of initial fixation (screw)
Disadv: Screw failure
Bone resorption secondary to hardware
Does not address soft tissue injury

c)Ligament reconstruction
Adv: Anatomic repair
No risk of metallic hardware failure or retention
Disadv: Less initial fixation strength
Harvest coracoacromial ligament

Chronic AC joint dislocations:

Type 1: nonoperative treatment will suffice
Type 2: initial conservative, on failure surgery.
Surgery involves distal clavicle excision combined with AC joint capsule reconstruction with CA ligament transfer
Type 3 to 6: Surgical treatment, distal clavicle excision with CA(coracoacromial) ligament transfer. The acromial attachment is detached and transferred to the resected end of clavicle


Complications:
1. Pneumothorax and pulmonary contusion are common with type VI injuries
2. Osteolysis of distal clavicle
3. Coracoclavicular ossification (disability is minimal)
4. AC joint arthritis is treated by Weaver Dunn technique: distal clavicle excision with CA(coracoacromial) ligament transfer
5. Complications of surgery include migration of pins as far as posterior mediastinal vessels and even carotids.
6. Failure of fixation is common

Role of Arthroscopy:
• The CA ligament can be released from the acromion during routine subacromial decompression and this will facilitate AC ligament reconstruction, including transfer of the coracoacromial ligament by decreasing the necessary size of the incision in the deltotrapezial fascia
• Wolf and Pennington described an all-arthroscopic technique of AC joint reconstruction(7)



Ref:

1. Nuber GW, Bowen MK. Acromioclavicular joint injuries and distal clavicle fractures. J Am Acad Orthop Surg 1997;5:11–18.
2. Lemos MJ. The evaluation and treatment of the injured acromioclavicular joint in athletes. Am J Sports Med 1998;26:137–144
3. Weaver JK, Dunn HK. Treatment of acromioclavicular injuries, especially complete acromioclavicular separation. J Bone Joint Surg [Am] 1972;54:1187-1194
4. Galatz LM, Williams GR, .Injuries to the acromioclavicular joint. In Rockwood and Green’s Fractures in adults, 6th Ed.
5. Kumar S, Sethi A, Jain AK. Surgical treatment of complete acromioclavicular dislocation using the coracoacromial ligament and coracoclavicular fixation: report of a technique in 14 patients. J Orthop Trauma 1995;9:507-510
6. Snyder S, Banas M, Karzel R. The arthroscopic Mumford procedure: an analysis of results. Arthroscopy 1995;11:157-164
7. Wolf EM, Pennington WT. Arthroscopic reconstruction for acromioclavicular joint dislocation. Arthroscopy 2001;17(5):558-563

Madelung's deformity

CONGENITAL SUBLUXATION OF THE
WRIST (MADELUNG’S DEFORMITY)

Pathogenesis (Brailsford):
 Stunted development of inner third of the growth cartilage at the lower end of the radius, due to still unknown cause.
 Growth of the outer two-thirds continues and, as a result, the radial shaft is bowed backwards, the interosseous space is increased, there is overgrowth of lower end of ulna and is subluxated backwards.

Soft tissue changes:• Abnormal tethering of soft tissues from the distal radius to the carpus and ulna.
• These have included aberrant ligaments and pronator quadratus muscle insertions
• Hypertrophy of the palmar ligaments, including the radiotriquetral and the short radiolunate ligaments and an anomalous volar ligament(Vicker’s ligament)

Clinical Features:

 Often bilateral, hence disability may not be identified early and hence late presentation is common
 Often seen for the first time in adolescence.
 Females>males.
 Early cases: mild symptoms of ulnocarpal impaction with power grip activities, and distal radioulnar joint incongruity with forearm rotation
 Flexion may be increased; other movements are restricted and may be painful.
 May be associated with Dyschondrosteosis (Leri Weil syndrome), Turner’s syndrome, Achondroplasia, Ollier’s disease

Vender and Watson Classification:
a) Post traumatic
b) Dysplastic
c) Genetic
d) Idiopathic



X-ray:
 Steep ulnar slope and deficient ulnar margin of radius
 Lunate uncovered.
 The carpus subluxates ulnar and palmarward and appears wedge shaped (lunate lies at the apex of the wedge)
 Increased width between the distal radius and ulna.
 Relatively long ulna compared to radius (positive ulnar variance).
 Decreased carpal angle.
 Triangularization of the distal radial epiphysis.
 Carpus migrates more proximal into the increasing diastasis between the radius and the ulna

Treatment

• In recent or acute cases, dorsiflexion of the wrist-maintained by a full arm plaster for 4 weeks.

Indications for surgery: Acute pain and deformity

Early presentation:
• In early-detected cases distal radial epiphysiolysis is done (Vickers and Nielsen et al.)
• Epiphysiolysis involves resection of the abnormal volar, ulnar physeal region of the radius and fat interposition. At the same time, any aberrant, tethering anatomic structures are excised
• Early presentation with marked deformity and complete lack of a lunate fossa for carpal support, needs combined radial and ulnar osteotomies. Alternatively ulnar and radial epiphysiodesis maybe done

Late presentation:
• Osteotomy of the lower end of the radius may be done. Options include dome osteotomy, dorsal radial closing-wedge osteotomy, or volar opening-wedge radial osteotomy and bone grafting
• Ulnar shortening procedure like the Suave-kapandji maybe useful, though there may already be deterioration of the articular cartilage, wrist ligaments, or triangular fibrocartilage, resulting in continued pain and limitation of motion postoperatively..

Ref:
1. Vickers D, Nielsen G. Madelung's deformity: treatment by osteotomy of the radius and Lauenstein procedure. J Hand Surg [Am] 1987;12(2):202-204
2. Ranawat CS, DeFiore J, Straub LR. Madelung's deformity. An end-result study of surgical treatment. J Bone Joint Surg Am 1975;57(6):772-775

Pigmented villonodular synovitis

PIGMENTED VILLONODULAR SYNOVITIS (PVNS)

Definition:
• Pigmented villonodular synovitis (PVNS) is a slow growing lesion of uncertain etiology arising from the synovial membrane, characterized by villous and nodular overgrowths of the synovial membrane of the bursa or the tendon sheath.
• The appendicular skeleton, especially large joints such as the knee and hip joints are frequently involved.
Synonyms: Until Jaffe in 1941 proposed the term pigmented villonodular synovitis this condition has been known as synovial xanthoma, synovial endothelioma/ fibroendothelioma, Benign fibrous histiocytoma, xanthomatous GCT, Myeloplaxoma, fibrohemosideric sarcoma , Sarcoma fusigigantocellulare.

History:
• 1852: 1st described as neoplastic process due to unrelenting growth pattern, by Chassaignac, eroding surrounding bone and joint tissue, & high recurrence rate post-resection.
• 1865: Simon described a focal form of PVNS
• 1909: Moser described a diffuse PVNS
• 1941: 1st reported & coined by Jaffe et al. as synovitis, shifting from neoplastic to inflammatory foci.

Prevalance:
• Age: 3rd-4th decades of life, rare in children
• Sex: no sex based predilection
• Incidence: 1.8 per million population
• no predilection for any laterality

Etiopathogenesis:
• repetitive trauma (50%) causing recurrent local hemorrhage to affected joint (cf:hemophilics show progressive erosive arthropathies).
• proliferation of the synovium of joints, tendon sheaths or bursae.
• It is a reactive condition, and not a true neoplasm.
• PVNS classically presents as a monoarticular disease, mimicking arthritis.
• Recurrent atraumatic haemarthrosis is a characteristic feature.
• Often aggressive, with marked extra-articular extension.

Types:

Monoarticular involvement (most common), occurs in two forms: localized and diffuse.
Two variants as described by Granowitz -

a. Localized form (LPVNS): focal involvement of the synovium
- Nodular / Sessile or Pedunculated masses.
- Hands & feet
b. Diffuse form (DPVNS) (more common): affects virtually the entire synovium, eg.
- Intra-articular PVNS tends to be of the diffuse form.
- Tendon sheath PVNS (Giant cell tumour of tendon sheath[GCCTS]), the nodular form.

Sites:
• MC site: knee joint, followed by the hip and shoulder.
• Knee:
- anterior compartment common
- mostly at meniscocapsular junction
- synovium in the region of the anterior horn of the medial meniscus is the most common site
- infrapatellar fat pad, suprapatellar pouch, intercondylar notch, anterior horn of the lateral meniscus, and the medial and lateral recesses of the knee have been reported.
• Uncommon : elbow, ankle, shoulder, foot, wrist
• Rare : spine, cervical involvement commoner than thoracic and lumbar

Clinical features:
o Pain (80%)
o Swelling(76%)
o Reduced range of movement(52%)
o Locking(16%)
o Instability/palpable mass(12%)

Type specific features:
• LPVNS:
- if untreated, causes continuous pain and discomfort, limiting ADLs
- at knee often present with signs and symptoms of meniscal pathology (locking, catching, and instability)
- episodic character of joint effusion—the patient may have completely symptom-free periods between exacerbations

• DPVNS:
- Slow, insidious onset of pain, swelling, and
- stiffness in the involved joint
- most or all joints involved
- swelling and pain more pronounced
- decreased range of motion of the affected joint
- poorly localized
- with sometimes extra-articular extension, either primary or recurrent.
- may encroach on major neurovascular structures.
- Osteoarthritis- continued inflammation and joint erosions lead to articular cartilage destruction, may finally need total joint arthroplasty.

Investigation:
Aspiration of joint: characteristically reveals a blood tinged brownish-stained aspirate.

X-ray:
• Soft tissue swelling will be marked due to haemorrhage and lobulated synovial tissue.
• May reveal cysts or erosions in the joint mimicking gout.
• Bony erosions are usually from without, especially in the hip
• periarticular erosions, with a thin rim of reactive bone
• Osteoporosis is characteristically absent
• Can affect the epiphysis
• Reciprocal bony lesions on opposite sides of the joint, despite articular preservation, are highly suggestive of PVNS
• Late feature of joint space narrowing indicates articular cartilage loss, is difficult to distinguish from primary OA.

MRI:
• ideal investigation
• nodular mass (periarticular or synovial) with bone erosion
• MRI is invaluable in early diagnosis and evaluating extent. Nodular synovial masses -low signal on T1/T2 sequences
• “dark on dark” on T1- and T2-weighted images

Sonography:
• Loculated joint effusions, Complex heterogeneous echogenic masses and markedly thickened synovium

Arthroscopy:
• direct visualisation of synovium
• Has both diagnostic and therapeutic value in resection of tumours
• Normal arthroscopic findings however does not exclude PVNS (Klompmaker et al)

Histolopathology:
• Synovium looks like a “shaggy carpet”.
• LPVNS is pedunculated, lobular lesion localized to one area of the synovium.
• On microscopy, Histiocytes, lipid laden macrophages, hemosiderin containing cells and frequent giant cells are seen.
• Subsynovial nodular proliferation of large round, polyhedral or spindle cells with prominent cytoplasm and pale nuclei.

Differential diagnosis
• Hemophiliac lobular synovitis (↑hemosiderin deposition, lacks lipidladen histiocytes and giant cells, which is classic indications of PVNS)
• Osteoarthritis
• Rheumatoid arthritis,
• Meniscal tear, or other ligamentous injury

Treatment:
• Synovectomy:
o Total synovectomy (open or arthroscopic):
- Open (anterior approach midline incision or medial parapatellar arthrotomy) for the diffuse form for the intraarticular component
- Arthroscopic synovectomy, has gained popularity, has several advantages over the open technique, preferred for LPVNS, shows higher recurrence in DPVNS.
- The standard anterior portals are not effective, whereas the accessory posterior portals are necessary
to accomplish total posterior synovectomy
o Vascular or neurologic injury may occur during this procedure, especially if there is posterior extra-articular
extension of the lesion or fibrosis after irradiation. Open synovectomy should be preferred in such cases
o Open posterior synovectomy (“lazy S-shaped” incision): done subsequently for extensions into the popliteal fossa.
• Local excision: for the nodular form (recurrence rare).
• Radiotherapy (3500- 4000 cGy) (Radiation induced synovectomy/ intra-articular radiation synovectomy using yttrium Y-90) has been used in the management of recurrences with varying success; side effect is soft tissue radionecrosis
• Advanced cases with secondary arthritis should be addressed with arthroplasty plus extensive synovectomy to decrease recurrence.

Prognosis:
• LPVNS: excellent prognosis, low recurrence rate if managed surgically, recurrence 8%.
• DPVNS: surgical excision difficult, recurrence rate of up to 46%.
• The debate continutes: malignant or inflammatory-
- Rare reports describe malignant transformation and metastasis, (presence of trisomy 7 and clonal DNA rearrangements reported).
- Bertoni et al reported eight patients with malignant PVNS; mortality rate was 50%.
- Oehler et al found strong support for its being a chronic inflammatory process and not noeplastic.
- Currently, data are inconclusive to prove PVNS as either malignant or inflammatory process.
- It shows neither cellular atypia nor abnormal mitosis, recent cytogenetic studies say that pathogenesis remains unresolved.

References:
1. Jaffe HL, Lichtenstein L, Sutro CJ. Pigmented villonodular synovitis, bursitis and tenosynovitis. Arch Pathol 1941;31:731–65.
2. Granowitz SP, D’Antonio J, Mankin HL. The pathogenesis and long-term end results of pigmented villonodular synovitis. Clin Orthop Relat Res 1976;114:335–51.
3. Oehler S, Fassbender HG, Neureiter D, Meyer-Scholten C, Kirchner T, Aigner T: Cell populations involved in pigmented villonodular synovitis of the knee. J Rheumatol 2000;27: 463-470.
4. Bertoni F, Unni KK, Beabout JW, Sim FH: Malignant giant cell tumor of the tendon sheaths and joints (malignant
pigmented villonodular synovitis). Am J Surg Pathol 1997;21:153-163.

Osteoid Osteoma

Osteoid Osteoma

 Most commonly involves the diaphysis of long bones especially femur and tibia, and the proximal femur is the most common site.
 50% of tumours involve the lower extremity
 Osteoid osteoma may have a unique ‘pathogenic’ nerve supply
 Three types have been described: Intracortical (80%), cancellous and subperiosteal
 The pain may be referred to an adjacent joint and when the lesion is intracapsular it may simulate arthritis with effusions ,spasms and contractures
 Occasionally pain precedes the appearance of radiographic changes, and leads to multiple incorrect diagnoses including neurosis
 In the spine, posterior elements of the lumbar spine is most commonly involved (next common thoracic spine). An associated scoliosis is often present
 If the nidus is in proximity to a nerve root, root irritation can develop.
 In the lumbar spine, this pain can present as sciatica and suggest the diagnosis of a herniated intervertebral disc
 Torticollis may be seen if the cervical spine is involved.
 Aspirin or nonsteroidal anti-inflammatory agents relieves pain secondary to a high concentration of prostaglandins in the nidus

Histology:
• There is a distinct demarcation between the nidus and the reactive bone
• The nidus consists of an interlacing network of osteoid trabeculae with variable mineralisation.
• The trabecular organization is haphazard and the greatest degree of mineralisation is in the centre of the lesion

Investigation:
• X rays: Central lytic nidus with extensive reactive sclerosis. The nidus is always less than 1.5 cm although the area of the reactive bone sclerosis may be larger.
• The radiolucent nidus may be obscured by dense sclerotic bone
• When the lesion is intramedullary there is less sclerotic bone
• CT scan is the investigation of choice
• Double density sign on bone scan (Focal areas of increased uptake with a second smaller area of increased uptake)
• MRI scans will show extensive edema, which may be confused with a marrow-replacing neoplasm and is therefore not recommended if osteoid osteoma is the suspected lesion

DD:
Bone island (enostoses):
‣ Mimic osteoid osteoma on X-rays but MRI changes are different from an Osteoid osteoma.

Treatment: If surgery is undertaken, it is important to eradicate the entire symptomatic nidus.
 Removal of a large amount of the surrounding sclerotic bone should be avoided because it can severely weaken the bone and may result in a pathologic fracture
 Intralesional resection by simple curettage of the nidus followed by high-speed burring is done often (Burr down technique).
 Intraoperative localization of the lesion may be done by technetium labeled methylene diphosphonate and detection by a Geiger counter
 If block excision is performed, intraoperative roentgenograms of the specimen are advised to document complete removal of the nidus
 CT-guided percutaneous resection for small tumours is becoming popular.
 Percutaneous Radiofrequency ablation is being tried. Under CT Guidance a radiofrequency probe is placed into the lesion and the nidus is heated upto 80degree C. This induces ionic agitation and frictional heat to cause tumor necrosis
 The patient may be also treated nonoperatively using NSAIDS. About 50% of the patients treated with NSAIDs will have their lesions burnt out with no further medical or surgical treatment necessary

Ref:
1. Cantwell CP et al: Current trends in treatment of osteoid osteoma with an emphasis on radiofrequency ablation. Eur Radiol 2004; 14(4):607.

Metal on Metal Bearing in Hip Arthroplasty

Metal on Metal (MoM)

- Are associated with decreased wear rate compared to conventional polyethylene
- Mixed film lubrication appears to be the operative mechanism in most metal-on-metal hip joints
- With metal-on-metal bearings, in contrast to polyethylene bearings, a larger-diameter bearing actually produces lower wear rates than does a smaller-diameter bearing
- Larger-diameter bearings have a greater arc of motion(and thus better ROM), which decreases the risk of impingement and also lessens the incidence of dislocation
- Alloys of cobalt (Co) and chromium (Cr) have been preferred for MOM bearings in THR because of their hardness.
- High chromium content provides good corrosion resistance
- There are two types of wear particles with MoM bearings: Co-Cr-Mo particles and chromium oxide particles
- It has been hypothesized that the Co-Cr-Mo particles are produced by the wear of the carbides on the bearing surfaces and the prosthesis matrix, and that the chromium oxide particles come from the passivation layer on the implant surface and possibly from oxidized chromium carbides

Metal hypersensitivity:
- all metals in a biological environment corrode; the ions released can combine with proteins and activate the immune system as antigens and elicit hypersensitivity responses
- the incidence of hypersensitivity is approximately 2 per 10,000
- are generally delayed cell-mediated responses
- ALVAL: are Lymphocytic infiltrations in the subsurface layer of the lining tissues, which were either diffuse or aggregated around small postcapillary vessels
- delayed type hypersensitivity should be considered when a patient with a well-fixed implant experiences chronic, aching pain with evidence of synovitis (an irritable range of motion) but has no objective evidence of infection
- If a modular MOM bearing is being considered, the use of substrates without Co-Cr (e.g., titanium) will allow revision of only the bearings in cases were hypersensitivity develops

What is New in Hip Resurfacing(Metal on Metal)?

-S. Glyn-Jones and H. Pandit reported in Dec 2009 JBJS B that incidence of ALVAL is higher in women especially if performed under 40 years of age.

-Factors significantly associated with an increase in revision rate were female gender, age under 40, dysplasia and small components.

-the higher revision rates in women could be due to increased prevalence of allergy in women because of wearing jewellery, increased ROM, which would be more likely to cause impingement, edge loading or different gait patterns