Legg Calve Perthes Disease

Legg Calve Perthes disease (LCPD) is a self-limiting condition caused by temporary interruption of blood supply to the growing proximal femoral epiphysis leading to necrosis, collapse and revascularization. Though the cause of vascular occlusion is not yet known, it leads to morphological and developmental changes in the proximal femoral head, femoral neck and acetabulum. The resultant irreversible deformation of femoral head, growth retardation, shortening of femoral neck, coxa vara and joint subluxation results in articular incongruity, altered joint mechanics predisposing the hip to premature osteoarthritis.

History

1905-         Kohler described radiographic changes of a patient similar to LCPD

1909-         Henning Waldenström described it as a benign form of tuberculosis.

1909-         Independently described by Arthur Thornton Legg from USA, Jacques Calve from France and George Perthes from Germany. 

1921-         Phemister described histologic findings suggestive of osteonecrosis in the specimens of a patient treated by curettage. He described creeping substitution during reconstitution phase.

1926-         Konjetzny first showed interruption of vascular supply.

1952-         Varus containment osteotomy described by Soeure of Belgium.

1962-         Salter described innominate osteotomy.

Epidemiology

Reported incidence range from 0.2 to 19.8 per 100000 population per year. Age of presentation of active disease range from 2 years to 11 years, but most commonly occur between 4-8 years of age. Boys are 4-5 times more commonly affected than girls. 10-15% of cases have involvement of opposite hip either simultaneously or at a later age. Boys 5 times more commonly affected than girls. Bilateral involvement is more common in girls.

Aetiology

Vascular occlusion leading to osteonecrosis in the growing epiphysis is the pathophysiologic pathway of LCPD. LCPD results from repeated episodes of vascular occlusion and hypercoagulable states may play a role in the pathogenesis. Vascular occlusion may be extrinsic or intraluminal. Vascular occlusion may be arterial or venous. Veins of proximal femur are susceptible to occlusion because of very thin walls, low flow rates, tortuous course around arteries and low pressure. Venous occlusion can lead to increased intraosseous pressure, reduced arterial blood flow, hypoxia and ischemic necrosis.

The exact cause of occlusion is not yet identified. The proposed mechanisms include trauma, genetic mutations, hypercoagulable states and transient synovitis. 

Higher incidence of factor V Leiden mutation, protein S deficiency, elevated factor VIII, and prothrombin G20210A mutation are reported especially in males. These conditions may result in thrombophilia or hypofibrinolysis. Multifactorial origin acting through a single shared common pathway is the currently favored model. Recently a single missense mutation of COL2A1 gene for type II collagen leading to replacement of glycine with serine at the codon 1170 have been reported in Asian families with multiple affected members.

A recent study reported coagulation anomalies in 75% of cases. The anomalies were protein C deficiency, protein S deficiency, elevated lipoprotein A and hypofibrinolysis. Other studies failed to demonstrate a similar finding.

Pathogenesis

Vascular occlusion leads to ischaemic necrosis. Ischaemic necrosis has biological and mechanical effects. Biologic consequence is a period of softness of head making it vulnerable for deformation and cessation of epiphyseal growth. Growth arrest can lead to femoral neck shortening and coxa vara. Greater trochanteric overgrowth of varying severity is seen in over 90% of patients with LCPD which can lead to Trendelenburg limp. Mechanical weakening leads to collapse due to repeated mechanical stresses. Mechanical effects are due to lose of sphericity of femoral head.

Biological effects are due to vascular compromise leading to cell death, followed by vascular ingrowth and bone resorption, finally ending with new bone deposition. Mechanical effects are due to softening, subchondral fracture, collapse, loss of sphericity, lateral extrusion, superolateral hinging, labral tear, stress concentration, articular cartilage degeneration and osteoarthritis. 

Ischaemic damage is followed by invasion of dead trabeculae by neovascularization, removal of dead trabeculae by osteoclasts followed by reossification by creeping substitution or repair by fibrovascular tissue which leads to weakening of femoral Head. Weakened femoral head collapses leading to flattening and deformation of head. Superolateral part of deformed head gets extruded outside the confines of acetabulum. Progressive deformation leads to lateral subluxation, articular incongruity and impingement. Altered joint forces leads to early arthritis in adulthood. 

The disease process evolves through the stages of avascular necrosis, fragmentation, reconstitution and healing. Extrusion of femoral head is the most important factor in deformation of femoral head. It occurs during the latter part of fragmentation stage. The final outcome is coxa magna (enlarged head and neck), coxa breva (shortened neck) and coxa plana (flattened head) with femoroacetabular impingement.

Associations

LCPD is associated with delayed skeletal age and low birth weight. Cranial structures are relatively spared from growth retardation than caudal structures with the foot showing greatest growth retardation. Low socioeconomic status is a strong association pointing towards environmental factors. Low concordance in identical twins is an evidence against genetic factors. Inguinal hernia, genitourinary malformations, undescended testes are reported associations. 

Clinical Features

Patients may present in childhood, adolescence or in adulthood. Usually asymptomatic initially till collapse or subchondral fracture develops. Child presents with painless limp and later complains groin pain or knee pain. Groin pain and lateral hip pain are the most common presentations. Lateral pain may be due to abductor insufficiency, trochanteric bursitis or trochanteric impingement. Groin pain may be due to impingement, instability or arthritic changes. Posterior pain is usually due to impingement.  

Gait may be antalgic or Trendelenburg type. Lumbar lordosis may be exaggerated due to flexion deformity. Anterior superior iliac spine may be at a higher level in presence of adduction deformity. There may be wasting of thigh and gluteal muscles. Tenderness over the anterior and posterior joint line may be present. Greater trochanter is usually thickened and elevated. Prominence of greater trochanter is due to lateral subluxation, muscle wasting, coxa vara and relative overgrowth of greater trochanter. Limitation of range of movements especially abduction and internal rotation seen. Fixed flexion deformity is seen. In the normal hip, rotations are more in 90 degree flexion than extension, called differential limitation of rotations. In LCPD, rotations are more limited in flexion than extension. Those children on skin traction may show near normal range of movements.

In adolescence, the hip is in healed stage and the physical findings depends on the amount of incongruity, impingement and femoral neck shortening. Residual deformity can cause intra-articular and extra-articular impingement. Many patients present with pain due to impingement. Shortening of variable degree is present. Adults present with pain and limitation of movement due to early onset osteoarthritis. Limitation of movements affects abduction and internal rotation, but other movements are affected as per severity of degenerative changes. External rotation deformity is seen in those with advanced degenerative changes. Flexion deformity and adduction deformity also is seen in those with severe incongruity or osteoarthritic changes.

Imaging

Diagnosis is usually made with the conventional x-rays, but radiological changes usually appears late. Hence recent trend is to rely on advanced imaging modalities such as perfusion MRI using gadolinium.

A correctly positioned AP view, false profile view of acetabulum and frog leg lateral view (Lowenstein view) should be taken in all patients suspected to have LCPD. AP view is taken in 15 degrees of internal rotation with the beam centred over a point midway between the superior margin of pubic symphysis and a line connecting both ASIS. If properly positioned the ilium, tear drop, obturator foramen should be symmetrical, the tip of coccyx should be in the midline in line with pubic symphysis and the distance from tip of coccyx to symphysis pubis should be within 2cm. 

The AP radiograph is used to measure the following radiographic parameters: lateral center edge angle, acetabular index, Shenton’s line and femoral head extrusion index. Look for the head at risk signs. Initial x-rays may be normal. Radiographic changes appear about 6 months after the first infarction has occurred. Earliest radiologic sign is a relatively smaller size of ossific nucleus of the involved head of femur.

Widening of medial joint space is found early seen (Waldenström sign). Widening of joint space due relative smaller size of ossific nucleus, lateral subluxation and thickening of articular cartilage.

Later the ossific nucleus becomes progressively sclerotic. Subchondral fracture may be seen. Subchondral fracture is called Caffey’s sign. Fragmentation and collapse leads to progressive deformation of femoral head. Lateral extrusion of head occurs with flattening of epiphysis. Shenton’s line shows superolateral migration of femoral head. Shenton’s line is considered to be broken if there is a step off of more than 5mm. Although changes are more noticeable in the proximal femur, acetabular changes are frequently present. Osteoporosis of acetabular roof, alterations in contour and change in dimensions is often seen. Acetabulum may show bicompartmentalization, ischium varum and early closure of triradiate cartilage. Acetabulum becomes shallow and misshapen. 

False profile view is taken with the patient standing and the body tilted 65 degrees to the x-ray beam, with the uninvolved side forward. On the false profile view of acetabulum measure the vertical centre edge angle. 

Catterall has described several radiographic findings as head-at-risk signs as indicators of poor prognosis. These are lateral extrusion, calcification lateral to the epiphysis, poorly ossified lateral part of epiphysis (Gage sign- Described by Courtney Gage in 1933), diffuse metaphyseal reaction (described by Smith in 1982) and horizontal growth plate. 

Measure the Heyman Herdon acetabular head index, Dickens and Menelaus femoral head extrusion index and Reimer migration index.

If containment surgery is planned, x-rays are repeated in hip abduction and in abduction-internal rotation to assess containment. Arthrography through an anterolateral or subadductorl access is an important adjunct to preoperative assessment as it visualizes the contour of articular cartilage and allows dynamic assessment of hip joint congruity. On the arthrogram assess the presence or absence of impingement, amount of subluxation manifested by medial clear space, presence or absence of hinged abduction and containment of femoral head within the confinements of acetabulum.

Bone scan findings precedes radiographic signs by 3 months. It is rarely used due to risk of radiation. CT is almost never used in children, but can be of use in adults to study impingement or to assess adequacy of columns before total hip replacement. 

Conventional radiography and x-ray based classifications have the limitation of inability to visualize the shape and deformation of cartilage. In addition, radiographic changes are present only in later stages of the evolution of LCPD. MRI has the advantage of visualization of cartilage and allows early detection of osteonecrosis. It is useful in detection of full extent and exact location of osteonecrosis, visualization of physis, chondral pathology and labral lesions. Epiphyseal changes are not associated with growth arrest in 76% of cases, but physeal and metaphyseal changes are associated with growth arrest.

MRI avoids ionizing radiation and is noninvasive. However, unenhanced MRI may fail to show changes in early stages of disease. Perfusion of the head can be studied using dynamic gadolinium enhanced subtraction MRI. MR perfusion index has been described as a measure of epiphyseal perfusion using digital image analysis of gadolinium enhanced subtraction MR images. It has been shown to correlate with femoral head deformity measured using conventional follow up x-rays. Necrosis extension, lateral extrusion, and the extent of physeal and metaphyseal involvement on MRI are important predictors of outcome. Horizontalization of labrum can also be identified on MRI which is indicative of significant femoral head deformation. Metaphyseal changes have been shown to be important predictors of physeal involvement and prognosis.

Classification

Classification can describe the extent and severity of disease at the time of presentation or its outcome. Classification help in predicting prognosis, deciding on treatment, comparison of treatment.

Waldenström Staging (1938)

Necrosis stage– Small sclerotic head with increased medial joint space.

Fragmentation stage– Epiphysis sclerotic, fragmented and collapsed.

Re-ossification stage– Reossification proceeding from lateral to medial and posterior to anterior

Healed stage– Density returned to normal with residual changes in shape and size of head.

Elizabethtown Classification

4 stages 

  1. Sclerotic 
    1. Without loss of height
    1. With loss of height
  2. Fragmentation
    1. Early
    1. Late
  3. Healing
    1. Peripheral – <1/3rd>1/3rd
  4. Healed

Catterall Classification (1971)

Group 1– <25% involvement. Anterior epiphysis only involved. No collapse, no metaphyseal involvement. Usually revascularised.

Group 2– Up to 50% involved. Collapse present. Central segment fragmentation and collapse. Necrotic portion appears sclerotic. Epiphyseal height maintained. Necrotic portion separated from viable portion on the lateral view in a characteristic ‘V’.

Group 3– >50% but not total involvement. Anterior, central and lateral involvement. Posterior part of head remains viable. Head-within-head appearance. Collapse present. Extensive metaphyseal changes with broadening of neck.

Group 4– Whole epiphysis affected. Collapse present. Mushroom shaped head. Extensive metaphyseal changes.

Described 4 “head-at-risk signs”

         1, Lateral subluxation

         2, Calcification lateral to the epiphysis

         3, Gage sign- Inverted V shaped defect laterally)

         4, Horizontal growth plate

         5, Diffuse metaphyseal reaction described by Smith in 1982

Salter Thomson Classification (1984)

It can be applied only in presence of subchondral fracture. Extent of subchondral fracture correlates with extent of subsequent collapse.

Group A– Subchondral fracture extent <50% of epiphysis.

Group B– Extent of subchondral fracture >50% of head.

Herring Lateral Pillar Classification (1992)

Done in the fragmentation stage. Epiphysis divided into lateral, central and medial pillars on the true AP view. Lateral pillar is the lateral 5-30% of epiphysis depending on the location of lucent line that separates it from the central necrotic area. If lucent line is absent, take the lateral 25% as lateral pillar. Maximum reduction in the height of lateral pillar measured in relation to normal side.  It is difficult to apply in bilateral cases and in the very young.

Group A– lateral pillar height fully maintained

Group B– Lateral pillar height >50% of normal. Good outcome if age is <9 years.

Group B/C– Lateral pillar height 50%, but poorly ossified. Added in 2004.

                            B/C1– Only 2-3mm width

                            B/C2– Minimum ossification

                            B/C3– Lateral pillar more depressed that central pillar

Group C– Lateral pillar height <50% of normal

All group A have good result. 2/3 of group B have good results. Only 25% of group B/C have good result. Only 1 in 8 with group C have a good result. 

Difficult to classify very young children. Needs about 7 months for proper classification. About 30% needs upgrading and only 4% remain in group A on subsequent follow up. Difficult to classify in bilateral cases.

Mose Classification

Done to assess outcome. Done on x-rays taken after 16 years of age. Classified into 3 types by placing Mose template with concentric circles at 2mm increments. Assess the sphericity of head.

Spherical

Nonspherical

Spherical but crescent shaped

Fasting scintigraphy classification(1980)

Grade 1– Decreased activity in <25% of head

Grade 2– Decreased activity in 50% of head

Grade 3– Decreased activity in 75% of head

Group 4– Decreased activity in whole of head

Conway Scintigraphy Classification (1992)

2 tracks. Track A of recanalization and Track B of neovascularization.

4 stages in each track.

Track A- 

         Whole head

         Lateral column

         Anterior and medial extension

         Complete

Track B

         Whole head

         Base filling

         Mushrooming

         Complete

Stulberg Classification 1982

Head shape divided into spherical (I or II), ovoid (III) or flat (IV or V). Subdivided according to coxa magna, steep acetabulum, short neck, 

I-      Normal

II-      Spherical – Within the circle by <2mm in both AP and lateral views. Coxa magna, short neck, acetabulum steep.

III-    Ovoid head. Out of shape by >2mm on either AP or lateral views

IV-    Aspherical congruency– Aspherical. Congruent.

V-      Aspherical incongruency– >1cm flattening on the superolateral weight bearing area. Incongruent.

I and II are spherical congruency, III and IV are aspherical congruency and V is aspherical incongruency.

Laredo Arthrographic Classification

Nature and extent of femoral head deformation and the severity of lateral extrusion are the most important factors that determine the prognosis. Radiographs show only the ossific portion proximal femoral epiphysis and may not represent the anatomical reality of the femoral head acetabular congruence. The understanding of the status of the cartilaginous portion is important especially in presence of persistent restriction of motion. However, it is an invasive procedure and difficult to repeat. Horizontalization of labrum is an important finding suggestive of deformation of head and it can be quantified by measuring the labral angle.

Group I – Normal hip

Group II

Femoral head larger than normal but spherical

Extrusion present at the neutral position and absent at 30 degrees’ abduction and slight internal rotation.

Group III

Femoral head larger than normal and ovoid

Extrusion present at neutral position and in 30 degree abduction and slight internal rotation.

Group IV 

Femoral head larger than normal and flattened

Extrusion is present at 30 degrees’ abduction and slight internal rotation 

Labrum loses its concavity and becomes elevated and straightened Hinged abduction present.

Group V

Femoral head larger than normal and saddle shaped

Extrusion is present at neutral position and in 30 degrees’ abduction and slight internal rotation.

Labrum is elevated and sometimes everted, with abnormal pooling of contrast medium at the saddle deformity area. 

Sphericity Deviation Score

Mark the medial and lateral edge of primal femoral growth plate on the AP and lateral views. Draw the maximum inscribed circle (MIC) touching these points without extending outside the femoral head. Mark the centre of the circle. Draw a second concentric circle as the minimum circumscribed circle (MCC) without extending inside the femoral head. Measure the difference between the radii of MIC and MCC (roundness error) on both AP and lateral views. Measure the difference between radii of femoral head on the AP and lateral views (ellipsoid deformation). The sum of roundness error on the AP and lateral views and the ellipsoid deformation is the Sphericity Deviation Score. SDS of normal hip is 0-3.8. If SDS at healing is less than 10, then the chance of hip having Stulberg I or II is high. If SDS is more than 20, then the hip is likely to have higher Stulberg grades at maturity.

Prognosis

60-80% of patients with LCPD have good outcome but it deteriorates on long term follow up. At a mean age of 45 years, 86% percentage of hips were found to be functioning and only 8% were found to have arthroplasty. But another report published later on the same group of patients at an average age of 53 years found that 40% of hips were replaced, 40% had functioning hips and 20% had osteoarthritic symptoms.  

Long term sequelae of LCPD are due to nonspherical head, short and broad neck, greater trochanteric overgrowth and labro-acetabular changes. Severity of these changes depends on the age of onset, gender, extent of femoral head necrosis, severity of femoral head deformation and method of treatment.

Age at onset between 5-7 years do better than those with age at onset more than 8-9 years. Catterall group III and IV patients with age at onset younger than 6 years may have poor outcome. In the multicenter study by Legg Perthes study group 59% of those aged less than 8 years at onset had a Stulberg II outcome while only 39% of those aged more than 8 years had a Stulberg II outcome. According to a study by Wiig from Norway 59% of those aged less than 6 years had a Stulberg I or II outcome and 38% of those above 6 years had a similar outcome.  

Age at the time of healing considered to be more important than age at onset. Age at follow up is also important with 86% having osteoarthritis at 65 years of age. About 50% of patients will ultimately need a total hip arthroplasty.

Lateral pillar classification also is helpful in prognosis determination. Stulberg I to II outcome found in 70-100% of lateral pillar A hips, 51-62% of lateral pillar B hips, 28% in B/C borderline hips and 13-30% of C hips.

Caterall grading also is significant in prognosis. 84% of Catterall 1 and 2 have a Stulberg I or II outcome and only 44% of Catterall 3 or 4 have a Stulberg I or II outcome.

Girls have poor outcome when compared to boys of same age due to more advanced skeletal age. Outcome is poor especially in girls aged more than 8 years. Overweight, longer duration for healing, persistent restriction of motion found to be associated with poor outcome.

Radiologically the following are important; extent of epiphyseal involvement, extent of metaphyseal changes, extent of lateral extrusion >20% and height of lateral pillar <50%. 

Method of treatment has a bearing on outcome in those aged more than 8 years with lateral pillar B or B/C with 73% of lateral pillar B treated by surgery having Stulberg I or II outcome while only 44% of those treated nonoperatively have a similar outcome. Greater trochanteric overgrowth is more common in lateral pillar C (44%) than in type B and B/C groups.41

 3 points from the Perthes Study Group regarding prognosis

1, Children with onset at less than 8 years are likely to have better outcomes. Generally lower age at onset have a better prognosis, but only half of those with age less than 5 years at onset with lateral pillar C have a good outcome.

2, Children more than 8 years at onset, if at least 50% of lateral pillar height maintained have better results if treated by surgery.

3, Outcome in Type C hips with less than 50% lateral pillar height is generally poor irrespective of treatment method.

Treatment

”TO BE CONTINUED”

Brachial Plexus Injuries in Adults

Introduction

The brachial plexus prone for injury because of following reasons.

  • The upper limb is connected to the axial skeleton mainly by the soft tissues, with the only bone connection of upper limb to axial skeleton being the clavicle.
  • Supraclavicular portion of brachial plexus is relatively superficial.
  • The shoulder girdle has a wide arc of movement.

These factors increases the risk  injury especially to the brachial plexus.

History

Homer described brachial plexus injury in the duel between Hector and Teucrus in Iliad.

1947- Seddon described nerve grafting.

1961- Yeoman and Seddon described intercostal nerve transfer.

1966- SICOT congress in Paris reached a consensus to discourage surgery for BPI due to discouraging results.

1970s- Work by Millesi in Vienna and Narakas in Lausanne demonstrated the utility of brachial plexus reconstruction

Anatomy

  • Dorsal roots (sensory) and ventral roots (motor) unite to form the spinal nerve.
  • The spinal nerve divides into dorsal and ventral rami. Dorsal rami supply the muscles and skin of paravertebral region.
  • The ventral rami of C5-C8 and T1 merge and decussate to form the brachial plexus with variable contribution from C4 and T2 between the anterior and middle scalene muscles. The brachial plexus can be divided to roots, trunks, divisions, cords and individual nerves.
  • Trunks are formed in the interscalene triangle. Cords are formed distal to the outer margin of first rib. Cords are named according to their relationship to the second part of axillary artery situated posterior to the pectorals minor.
  • C5 and C6 ventral rami unite to form the upper trunk (C5-6). C7 continues as middle trunk  (C7). C8 and T1 unite to form the lower trunk (C8-T1).
  • Each trunk divides into anterior and posterior divisions. The anterior divisions of upper and middle trunk unite to form the lateral cord (C5,6,7). The anterior division of lower trunk continue as medial cord (C8-T1). Posterior divisions of upper, middle and lower trunks unite to form the posterior cord.
  • Individual nerves may arise from the roots, trunks or cords of brachial plexus.
  • No nerves arise from the divisions of brachial plexus.
  • The phrenic nerve, long thoracic nerve and dorsal scapular nerve arises from the roots.
  • Long thoracic nerve arises from C5, C6 and C7 roots and supplies the serratus anterior.
  • Dorsal scapular nerve arises from C5 root and supplies the levator scapulae and the rhomboids major and minor.
  • The nerve to subclavius (C5) and suprascapular nerve (C5,6) arise from the upper trunk.
  • Suprascapular nerve (C5,6) supplies the supraspinatus, infraspinatus and teres minor.
  • Lateral cord (C5,6,7) gives rise to lateral pectoral nerve, musculocutaneous nerve  and lateral root of medial nerve (Mnemonic- LML).
  • Medial cord (C8,T1) gives rise to medial cutaneous nerve of arm, medial cutaneous nerve of forearm, medial root of median nerve, medial pectoral nerve and ulnar nerve (Mnemonic- MMUMM).
  • Posterior cord gives rise to subscapular nerve, thoracodorsal nerve, axillary nerve  and radial nerve (Mnemonic- STAR).

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Plantar Plate Insufficiency or Rupture (Turf Toe)

Anatomy

  • During normal gait, MTPJ has to sustain more than 40 to 60% off bodyweight, during normal athletic activities this increases to 2-3 times the bodyweight. During running jump MTPJ sustains eight times the body weight.
  • Metatarsophalangeal joint (MTPJ) is statically stabilised by the plantar plate and the collateral ligaments.
  • Dynamic stability for the first MTPJ is provided by the short flexor complex, which is composed of medial and lateral bellies of flexor hallucis brevis, adductor hallucis and abductor hallucis muscles and the medial and lateral sesamoid bones and their ligaments.
  • Plantar plate is the trapezoid shaped thickening of the MTPJ capsule at the weight bearing plantar aspect.
  • It is a fibrocartilaginous structure that resists hyperextension and provides stability to the MTPJ.
  • It is the major stabiliser of the MTPJ.
  • It provides a smooth gliding surface for the flexor tendons inferiorly and metatarsal head superiorly.
  • Proximally it is inserted into the metatarsal neck.
  • Distally to the base of proximal phalanx by medial and lateral longitudinal bundles.
  • It receives attachment from collateral ligaments, deep transverse metatarsal ligaments and vertical fibers of plantar aponeurosis.

Pathology

  • Degenerative or traumatic rupture of plantar plate is an under-recognised cause of metatarsalgia.
  • Degenerative rupture of plantar plate especially in the second MTPJ can lead to metatarsalgia with synovitis, which if untreated progresses to hammer-toe, claw-toe or crossover-toe deformity.
  • In 2/3rd of cases the second toe is commonly involved as it tis the longest.
  • Long term use of high heel foot wear may be a cause in older women as it causes chronic
  • Lesions can cause metatarsalgia, instability, deformity and dislocation.
  • Deformity may be in the sagittal plane such as hammertoe and claw toe or coronal plane such as crossover toe..
  • During the heel-off and toe-off of stance phase of gait, the MTPJ becomes dorsiflexed. Dorsiflexion is passively resisted by the plantar plate and actively by the intrinsic musculature.
  • With insufficiency of plantar plate, dorsal subluxation of MTPJ occurs. The interossei is displaced dorsally leading to hyperextension of MTPJ. The medially located lumbrical causes adduction deformity. Attenuation of collateral ligaments also contributed to the development of coronal plane deformity.
  • Majority of cases have an insidious onset and is seen in sedentary older women.
  • It can be seen in young athletic males after trauma.
  • It can also be seen as a secondary deformity in association with hallux valgus, hallux varus, pes planus and hallux rigidus.
  • The term Turf Toe introduced by Bowers and Martin in 1976 for injuries of the plantar plate of first metatarsophalangeal joint (MTPJ) of great toe seen in athletes playing on artificial turfs using lighter and flexible shoes.
  • Coughlin coined the term ‘second crossover toe’ in 1987 to describe the coronal plane deformity.
  • Hyper-dorsiflexion of the MTPJ is the most common mechanism of injury.
  • Causes distractive forces on the plantar plate, sesamoid complex and toe flexors.
  • In the big toe, the plantar plate rupture occurs distal to the sesamoids.
  • Rarely tissue disruption occurs through the sesamoids producing sesamoid fracture.
  • Injury may be partial or complete. It may extend to the collateral ligaments in presence of varus or valgus moment.
  • Hyper-plantarflexion injury is called Sand Toe as it is common in beach volleyball.

To read the complete article

https://learningorthopaedics.com/plantar-plate-insufficiency-or-rupture-turf-toe/

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Femoroacetabular impingement

Definition Early pathological contact between bony prominences of femur and acetabulum during hip motion due to a variety of morphological conditions leading to pain and chondrolabral damage predisposing the patient to early osteoarthritis of hip.

Introduction

• First described in 2003 by Prof Reinhold Ganz from Bern Hip Group, Switzerland.

• Impingement may be intra-articular or extra-articular.

• Intra-articular impingement may be of 3 types

○ Cam

○ Pincer

○ Combined-86%

• Abnormal morphology and / or motion is required for clinically relevant impingement to occur.

• In addition a subluxating impingement also has been described by Leunig in 2001 in patients with shallow and dysplastic acetabulum.

Cam type impingement

• Loss of normal head neck offset is the underlying cause.

• The hump at the femoral head neck junction and the loss of normal concavity of the superior border of neck of femur is called pistol grip deformity.

• Anterior hump causes outside-in abrasion of labrum and cartilage in the anterosuperior part of acetabulum on flexion and internal rotation.

• Mismatch between femoral head and acetabulum leads to abutment of aspherical head and acetabulum rim leading to shear stresses which causes injury to the labrum and cartilage.

• Chondrolabral separation, cartilage delamination and chondral defects develop leading to osteoarthritis.

Pincer type impingement

• Acetabular overcoverage is the underlying cause.

• Overcoverage may be localized or generalized.

• Overcoverage may be due to increased acetabular depth, abnormal version of acetabulum or localized bone overgrowth.

• Leads to labral damage, ossification of labrum and cartilage damage over a circumferential narrow strip at the rim of acetabulum.

• Impingement may lead to subluxation of head in the opposite direction leading to contre-coup cartilage lesions.

Clinical assessment

• Young in their 20-40s.

• Presents with groin pain in the sitting position.

• Pain during or after sports activities

• Internal rotation and flexion are typically limited.

• Anterior impingement test- Groin pin on forced internal rotation and adduction in 90 degrees of  flexion.

• Posterior impingement test- Pain on hyperextension and external rotation of hip.

• Drehmann’s sign- Unavoidable passive external rotation on flexion (axis deviation) due to anterior impingement.

Imaging

• Anteroposterior and lateral views of the pelvis with both hips are taken.

• Identify the abnormal morphology of acetabulum and femur.

• Identify labral and cartilage damage.

• Herniation pits or Pit’s pits are seen in FAI.

• In cam impingement, the characteristic chondrolabral damage is seen in the anterosuperior part of acetabulum.

• In pincer impingement chondrolabral damage is seen posteroinferiorly.

• Quantify the degree of osteoarthritic changes

○ As positioning for x-rays can alter the measurements first ensure proper positioning of x-rays.

○ Acetabular coverage- CE angle, Acetabular index, Extrusion index

○ Acetabular depth- Kohlers line

○ Acetabular version

   § Posterior wall sign- Posterior margin of acetabulum lies medial to the centre of femoral head.

   § Cross over sign- Posterior margin of acetabulum crosses the anterior margin and the inferior part of posterior margin lies medial to the anterior margin.

   § Ischial spine sign- Prominent ischial spine projecting medial to the pelvic brim is a sign of retroversion of acetabulum

  ○ Femoral head neck asphericity.

   § Alpha angle- Described by Notzli. <50 degrees. >55 degrees indicates loss of femoral head neck offset. Measured ideally on the radial slices taken along the axis of femoral neck. Angle between the axis of femoral head and neck and the line drawn between center of femoral head and the head neck junction.

   § Head neck offset less than 10mm.

  ○ Femoral neck shaft angle

• Varus and valgus deformity of proximal femur may also may contribute to the development of impingement.

• Torsional deformity especially of the acetabulum is an important cause of impingement.

• Conventional MRI with orthogonal slices cannot fully visualize the labral and chondral lesions of FAI.

• MR Arthrography with radial slices is the gold standard for assessment of FAI.

• Delayed Gadolinium-enhanced MRI of cartilage (dGEMRIC) allows quantitative assessment of chondrolabral damage.

Treatment

• Depends on the age and activity profile of the patient.

• Asymptomatic individuals generally doesn’t need treatment.

• If significant osteoarthritic changes are present then total hip replacement is the treatment of choice.

• In the absence of OA changes; treatment depends on the type of impingement, location of impingement and degree of acetabular and femoral version.

• Aim of treatment in cam impingement is restoration of sphericity of the femoral head by reshaping the head neck junction.

• Cam impingement is treated by osteochondroplasty.

• Isolated anterosuperior cam impingement can be treated by arthroscopy.

• Cam impingement close to the site of entry of epiphyseal vessels, posterior cam and multiple pathologies need open treatment by safe surgical dislocation.

• Safe surgical hip dislocation is the gold standard in the treatment of FAI.

• Lateral approach through the Gibson interval between gluteus medius and gluteus maximus utilized.

• Z- capsulotomy with preservation of labrum, short external rotators, pyriformis and the medial circumflex artery.

• Anterior limb of capsulotomy is close to the femoral attachment of capsule and the superior limb is at the acetabular attachment of capsule.

• Aim of treatment in pincer impingement is to reduce acetabular overcoverage.

• Pincer impingement needs careful assessment of acetabular version.

• Severe retroversion of acetabulum needs periacetabular osteotomy to restore normal anteversion of acetabulum.

• If acetabular version is normal then pincer impingement is treated by rim trimming and labral reattachment.

Basics of radiation safety for the orthopaedic surgeons

Use of c-arm is now an essential part of orthopaedic practice.  Use of C-arm fluoroscope in orthopaedics has improved patient outcomes by improving precision in surgery and by reducing surgical trauma by permitting minimally invasive techniques.


 Radiation Physics


 

Within the x-ray source an electrically heated filament produces electrons. These electrons are accelerated by a high voltage towards an anode made of high atomic weight elements such as tungsten. When the high energy electrons hit the tungsten and gets decelerated a small number of x-ray photons are emitted and the rest is converted to heat. The number of electrons depends on the strength of the electric current in milliamperes (mA). The maximum kinetic energy of the electrons is expressed as kilovolts peak (kVp). Higher mA produces more x-ray photons and higher kVp produces higher energy x-ray photons with greater penetrability. Higher mA increases the brightness of the image. Higher kVp may reduce the contrast of the image.

As the beam leaves the x-ray tube the rays diverge leading to reduced radiation with increasing distance. As the relationship between radiation and distance is by inverse square law; even small increase in distance can reduce radiation by a large percentage.


 

Fate of x-ray within the human body


When x-rays are beamed towards the human body they may three outcomes depending on the tissue electron density, tissue thickness and the x-ray beam energy.

  1. Completely penetrate the body and emerge at the opposite end to be detected by the film or detector. (1% of the beam during fluoroscopy)
  2. Completely absorbed by the tissue.
  3. Scattered by the tissue.

History


After the discovery of xrays by Roentgen in 1895, its potential benefits in the medical field was immediately recognised but the identification of its deleterious effects took a longer time. Radioactivity was discovered in the same year by Becquerel and its usefulness in the treatment of malignancy was recognised early due to its deleterious effects. In the year 1900, Albers Schonberg advised reduced frequency of exposure, use of lead shielding, gap of more than 30 centimetres from source as safety measures when working with radiation. In 1928, roentgen was accepted as the quantitative measurement for radiation exposure. International X-ray and Radium Protection Committee was formed in 1928.  It was renamed later as International Commission on Radiological Protection (ICRP). Its aim is to advance the science of radiation protection. It has published several guidelines for radiation protection.


 

C-Arm


C-arm is an x-ray unit that allows alteration of angle and rotation of X-ray source and detector to permit imaging without changing the position of the patient. It was introduced in 1955. It is comprised of an X-ray generator and a image intensifier. The X-rays strike a fluorescent screen which glows according to the strength of the radiation. C-arms use caesium iodide for the fluorescent screen which converts the X-ray photons into photons in the visual spectrum by its luminescence property. A photocathode made of an antimony caesium compound situated beneath the fluorescent screen captures the glow and amplifies the luminance. In C-arms with flat panel detector the X-Rays are converted digitally into a visible spectrum.


Risks of ionizing radiation


Ionising radiation is potentially hazardous to the personnel and patient. Ionising radiation is classified as a carcinogen by the World Health Organisation. X-ray photons absorbed are a source of injury to the patient and the scattered rays is a potential source of injury to the personnel.

Risk of radiation injury is increased with higher doses and longer exposure times. The harmful effects may be for the individual or his descendants. They may be classified as somatic or genetic. Biological effects of radiation are classified into stochastic effects and deterministic effects. Stochastic effects may be malignancy or genetic defects. Stochastic effects like cancer and genetic defects can occur at any dosage levels. Deterministic effects occur when the threshold level is exceeded and their severity depends on the dosage. Deterministic effects are due to excessive cell death and can be erythema, epilation, skin necrosis or cataract formation.


 

Radiation Protection Principles


The radiation protection guidelines assume that the health risk of radiation increases with the dose which is called linear no-threshold hypothesis. This has lead to the formulation of ALARA (As Low As Reasonably Achievable) principle as the key to radiation safety guidelines.

As per current laws, the hospital is responsible for the protection of those exposed to ionising radiation within the hospital premises including the patients, personnel and the public. Medical procedures that need use of ionising radiation should be justifiable, safe and should be performed by trained person using appropriate equipments and methods. Any breach of safety regulations prescribed by laws is an offence.

There should be protocols and training of personnel to ensure radiation safety. Dosage restrictions should be stipulated and appropriate monitoring badges should be provided. An audit of the use of ionising radiation, compliance with safety protocols and exposure dosage monitoring is required as per the guidelines. Exposure time should be recorded in the patient case sheet. As the hazards are not immediately evident and also due to ignorance, the compliance with the safety measures is often alarmingly low.

The three basic factors that determine the safety are the exposure time, distance from source and shielding. In simple terms; reduce the exposure time, increase the distance from the source and use appropriate shielding. The exposure to the surgical team is actually greater than in conventional radiography due to the reduced distance, less shielding and exposure time especially during difficult procedures. Lead aprons, thyroid shields and leaded eyewear are a must for personal protection. Though heavier, wraparound aprons are better.

Exposure time and X-ray field size should reduced to the the maximal extent possible. X-ray beam should be well collimated. Simulated skin entrance and exit exposure levels and the scatter radiation levels should be measured by a qualified physicist at all occupied areas around the c-arm to determine the type, number and location of the personal radiation monitors to be used. Ideally a whole body monitor badge should be worn under the lead apron and a badge should be worn outside the thyroid shield. A wrist badge should be worn on the hand closest to the beam to monitor the extremity exposure.

The exposure to the patient is determined by distance from the source, thickness of the patient, kV, mA and the exposure time. Thicker the patient more is the exposure. The closer to the source greater is the exposure. Patient exposure can be reduced by reducing the duration of exposure, increasing the distance from the source and reducing the field size.


 

Practical Steps to improve radiation safety


 

X-ray source
  • The X-ray source should be kept as far away from the patient as possible. If the source is closer to the patient the beam is concentrated on a small area increasing the chance of injury.
  • The source should be kept below the operation table whenever possible. The main source of radiation to the personnel is scattering of beam by the patient. When the source is kept below the radiation is scattered on to the ground.
  • When taking lateral or oblique view keep the source away from the personnel. The image intensifier should be towards the personnel.
  • Collimate down to the area of interest. This will decrease the amount of tissue irradiated and the scattering.
Image intensifier
  • Keep it as close as possible to reduce the scattering, to reduce the patient dosage and to obtain a larger field of view.
  • Personnel should stand on the side of image intensifier to reduce exposure to scatter rays.
Technique
  • Use the lowest mA possible  as the higher tube current increases the dosage.
  • Larger kVp increases the penetrability of beam allowing the use of a lower mA. But large kVp may reduce contrast.
  • Reduce the exposure time to the minimum. Normal mode fluoroscopy produces 1 to 10 R/min (0.01 to 0.1 Gy/min). HI or boost mode produces 10 to 20 R/min (0.1 to 0.2 Gy/min).
  • Avoid pulse mode and continuous mode.
  • If needed. use pulse mode than continuous mode. Continuous mode increases the dose exponentially. Radiation is 10-20 times more during continuous mode.
  • When using pulse mode, use a lowest frequency possible.
  • Reduce the magnification to the minimum as both digital and geometric magnification increases the dosage. Dose increases at the rate of square of magnification.
  • Radiation is higher in larger patient as a bigger mA increasing the dosage and scatter.
Personnel

Remember that scatter rays are the main source of radiation to the personnel. Injury from scatter rays can be reduced by use of shields and by increasing the distance from the source. Remember that the lens of the eye and the thyroid are most vulnerable to radiation injury.

  • Use protective aprons, thyroid shields and lead goggles.
  • Exposure from a radiation source decreases by the inverse of the distance squared. Hence stay as far away as possible from the X-ray source.
  • Stand on the side of image intensifier as far as possible.
  • Use dose monitors.
  • Use portable shields if available.
  • Preoperative planning an careful checking of the previous images can help to reduce the number of exposures.
  • Annual dosage limit for hospital workers is 500 mrem for the whole body, 1500 mrem for the eyes and 5000 mrem for all other organs. Dosage limit for pregnant women is no more than 500 mrem (5 mSv) during the entire gestational period and no more than 500 mrem in a month.
Protective shielding
  • Full wrap around type protective gowns are recommended.
  • It should have 0.50 mm Pb in the front panels and 0.25 mm Pb in the back panels.
  • Use protective  thyroid shields with an equivalent of 0.50 mm Pb.
  • Use of leaded glasses to protect the eyes.
  • Protective gloves should have at least a 0.25 mm Pb equivalency. But remember that these gloves do not protect the hands if placed within the primary beam.
  • They should be checked yearly for efficiency.
  • After use the protective aprons and thyroid shields should be stored properly to prevent damage.
  • Lead aprons and thyroid shields with 0.5mm lead thickness provide 85%–95% attenuation of scattered x-rays.

 

Terminology


Absorbed dose- The total amount of radiation energy absorbed per volume of tissue exposed.

Effective dose- Depends on the proclivity of tissue or organs exposed to develop stochastic effects and the type of radiation involved.

Tissue-weighting factors is high for breast tissue and ovaries as they are more prone for stochastic effects.

Entrance surface dose

Dose-area product

Collective dose

Background effective dose (BRE) is the radiation from natural sources in the general population. In the United States is approximately 3.1 mSv per year. It is up to 70 mSv per year in Kerala, India due to the naturally occurring thorium coated monazite sand. A pelvic radiograph has an effective dose of ~0.6 mSv hence the BRE = 71 days.

kVP – Kilovolt peak

mA- Milliampere

As per the newer guidelines  gray (Gy) replaces roentgen (R) for exposure. The  gray (Gy) replaces the  rad (rad) as the unit of absorbed dose. And the  sievert (Sv) replaces the  rem (rem) as the unit of equivalent dose.

Gout

  • Gout is an inflammatory arthritis caused by deposition and accumulation of monosodium urate crystals in tissues, mainly synovium, cartilage and skin with or without symptoms as a result of long standing hyperuricemia.
  • 90% of gout is due to under excretion and 10% is due to increased synthesis.
  • The stages of gout are hyperuricemia, asymptomatic gout, acute gout, inter-critical gout and chronic gout.
  • It is often associated with metabolic syndrome with insulin resistance, hypertension and diabetes mellitus.
  • Gout and asymptomatic hyperuricemia is associated with significantly elevated risk of chronic lifestyle diseases such as obesity, hypertension, ischaemic heart disease, type 2 diabetes, chronic kidney disease etc.
  • Nephropathy and disorders associated with increased cell turnover can be associated.

Metabolism


  • Uric acid is the end metabolite of purine metabolism in humans.
  • In other species, presence of the enzyme called uricase converts uric acid into highly water soluble allantoin.
  • In humans, the uricase gene is inactivated by the presence of 2 mutations.
  • The level of uric acid in humans is 10 times higher than other species due to the absence of uricase.
  • It is a weak acid and at the physiologic pH exists in the ionic form called urate.
  • Uric acid levels depend on the dietary intake, synthesis and excretion.
  • The limit of solubility of urate is 6.8mg/dL.
  • When exceeded, urate crystal deposition occurs in tissues.
  • Solubility of urate is determined by the following factors
    • pH
    • Body temperature
    • Level of hydration
    • Presence of nucleation factors
    • Concentration of cations

Clinical Features


  • Episodic urate crystal induced acute inflammation of joints, tendons and bursa is the classic picture of acute gout.
  • Acute attack which peaks within just 6–12 hours with overlying erythema is highly suggestive of crystal inflammation though not specific for gout.
  • In recurrent podagra with hyperuricemia, a clinical diagnosis is reasonably accurate but not definitive without crystal confirmation.
  • Lower limbs are more commonly affected than upper limbs.
  • Peripheral joints are more commonly affected than central joints.
  • First metatarsophalangeal joint is the site of presentation (Podagra) in more than 50% of cases. Other sites of first attack are the tarsal joints ankle and knee.
  • More than 80% of the site of first episode is in the lower limbs.
  • The first episode is monoarticular in 90%.
  • Polyarticular onset is seen in less than 1%.
  • Olecranon bursa is the commonest site of first attack in the upper limb.
  • First metatarsophalangeal joint is affected in more than 80% of patients with uncontrolled or untreated gout.
  • Acute attacks are preceded by prodromal symptoms such as mild pain, limitation of motion and discomfort.
  • Acute attacks have an abrupt onset with rapid development of acute inflammation with excruciating pain during the first 24-48 hours.
  • Provocative factors for acute attacks include severe dietary restriction, high purine diet, local trauma and initiation of treatment.
  • Sudden drop in uric acid level results in disintegration of solid aggregations leading to local inflammation.
  • Macroscopic collections of urate crystals is called tophi. More commonly seen in areas subjected to pressure or friction.
  • Limitation of joint movement is due to accumulation of tophaceous deposits in the joints and periarticular tissues.
  • Intraarticular tophi may present with mechanical symptoms mimicking meniscus tear or loose body.
  • Rupture of intradermal tophi may mimic pustules.
  • Persistent joint swelling is called chronic gouty arthritis. It is due to chronic granulomatous inflammation induced by urate crystals. X-rays usually show only minimal destruction, but MRI or USG show extensive soft tissue deposits.

Natural history of untreated gout


  • More than 75% develop subsequent acute attacks.
  • Frequency of attacks increase in 50%.
  • Severity of attack increases in 30%.
  • Polyarticular involvement develops in 40%.
  • Tophaceous burden increases.

Investigations


Diagnostic investigations are done for

o          Confirmation of gout.

o          Determination of burden of disease.

o          Identification of complications.

o          Identification of other associated rheumatic conditions.


Confirmation of diagnosis

  • Demonstration of MSU crystals in synovial fluid or tophus aspirates is the gold standard for the diagnosis of gout.
  • Synovial fluid should be send for total count, differential count, analysis, gram stain, bacterial culture and biochemical analysis.
  • MSUC are water soluble and is dissolved if preserved in formalin, hence tissue samples to be examined for urate crystals should be fixed in 100% alcohol.
  • In all synovial fluid samples obtained from inflamed joints for diagnosis, search for MSU crystals.
  • During the intercritical period, definite diagnosis can be made by identification of MSU crystals in the asymptomatic joints.
  • Gout and sepsis may coexist, hence do gram staining and culture
  • Serum uric acid levels alone do not confirm or exclude gout, as many with hyperuricemia do not develop gout, and the serum levels may be normal in many with acute attack.
  • In those with a family history of young onset gout, onset of gout under age 25, or with renal calculi determine the renal uric acid excretion.

Determination of burden of disease

  • Number of acute exacerbations.
  • Number and location of joints ever involved by acute attacks.
  • Presence, size, and location of superficial tophi.
  • Persistence of pain, joint swelling, limitation of motion, and deformities.
  • Short 4-joint USG of both knees and first metatarsophalangeal joints.

Look for comorbidities such as obesity, hyperglycaemia, hyperlipidaemia and hypertension.


Imaging


  • Conventional x-ray
  • Ultrasonography
  • Three-dimensional (3D) multislice imaging via computed tomography (CT),
  • Dual-energy computed tomography (DECT)
  • Magnetic resonance imaging (MRI)

Radiography

  • Radiographs are not useful in confirming the diagnosis of early or acute gout.
  • Play a minor role in diagnosis.
  • Nonspecific initially.
  • Acute gout attack produces soft tissue swelling.
  • Asymmetric erosive arthropathy especially of the first MTPJ is the characteristic appearance of chronic gouty arthritis.
  • Gouty deposits cause well corticated erosions with typical overhanging margins.
  • New bone formation can be seen in the form sclerosis, osteophytes, bony spurs and, rarely, periosteal deposition and ankylosis.

CT Scan

  • Multislice helical CT scanning can show tophaceous deposits with a typical density of 160–170 Hounsfield units. They are found close to the erosions extending into the soft tissues.

Dual Energy CT

  • Uses 2 X-ray tubes arranged perpendicular to each other using different voltages. It has the potential to detect intra-articular and extra-articular urate crystals which would have been otherwise undetectable.

High resolution ultrasound scan.

  • Serial high resolution ultrasound may be used to assess response to treatment.
  • Highly sensitive for detection of erosions.
  • Double contour sign seen

Diagnosis Criteria


Rome criteria – 1963

(2 of 4 required for diagnosis)

  • Serum uric acid > 7mg/dl in males and >6mg/dl in females
  • Tophus
  • Urate crystals demonstrated in the synovial fluid
  • History of recurrent attacks of joint swelling of abrupt onset which resolves within 2 weeks.

New York criteria – 1968

  • Demonstration of urate crystals in the synovial fluid or tissue.

OR

More than 2 of the following criteria.

  • Tophi
  • History or observation of podagra.
  • History or observation of at least 2 attacks of painful limb swelling of abrupt onset which resolves within 1-2 weeks.
  • History or observation of good response to colchicine within 24 hours.

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