conditions in and around the hip joint

8/7/2019 conditions in and around the hip joint

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conditions in and around the hip joint

Adductor strain

Hamstring strainIT band strain

Piriformis syndrome

Trochanteric bursitis

CDH

osteitis pubis

Coxa vara & valga

Perthe¶s disease

AVN



Adductor (groin) strain



Adductor (groin) strain

An adductor (groin) strain is a common problem among many individualswho are physically active, especially in competitive sports.

The most common sports that put athletes at risk foradductor strains arefootball, soccer, hockey, basketball, tennis, figure skating, baseball,horseback riding, karate, and softball.1

Hip adductor injuries occur most commonly when there is a forced push-off (side-to-side motion). High forces occur in the adductor tendons whenthe athlete must shift direction suddenly in the opposite direction. As aresult, the adductor muscles contract to generate opposing forces.

One common cause of adductor strain in soccer players has beenattributed to forceful abduction of the thigh during an intentionaladduction. This type of motion occurs when the athlete attempts to kickthe ball and meets resistance from the opposing player who is trying tokick the ball in the opposite direction. To a lesser extent, jumping alsocan cause injury to the adductor muscles, but, more commonly, itinvolves the hip flexors. Overstretching of the adductor muscles is a lesscommon etiology



Pathophysiology

The hip adductors are a powerful muscle group. They consist of theadductor magnus, minimus, brevis, and longus. The gracilis andpectineus muscles also are included. All of the adductor muscles areinnervated by the obturator nerve (L2-L4) except the pectineus, whichis innervated by the femoral nerve (L2-L4). The adductor magnus alsois innervated by the tibial nerve (L4-S3).

The musculotendinous junction is thought to be the most common siteof injury in a muscle strain. the sarcomeres near the junction are less

elastic than those found at the central portion of the muscle. Themusculotendinous junction is likely to be vulnerable to indirect muscleinjury that results from excessive force.



Mortality/Morbidity

Improper management of acute adductor strains or returning to play beforepain-free sport-specific activities can be performed may lead to chronic injury.

Chronic adductor strain: ± Generally, symptoms are more diffuse with typical complaints of pain and stiffness in

the groin region in the morning and at the beginning of athletic activity. Pain andstiffness often resolve after a period of warming up but often recur after athleticactivity.

± Typical findings include tenderness at the origin of the adductor longus and/or thegracilis located at the inferior pubic ramus and pain with resisted adduction.

Improper management of acute adductor strains:

± According to a study by Renstrom and Peterson, 42% of athletes with groin muscle-tendon injuries could not return to physical activity after more than 20 weeks followingthe initial injury.

± This prolonged length of time seems to indicate the importance of proper management of these injuries in the acute stage.



History

Groin pain can represent a number of different diagnoses, and all differentialdiagnoses should be kept in mind when assessing the patient. Obtaininformation about the mechanism of injury and loss of function, as well as about

the location, quality, duration, and severity of pain. The aggravating andalleviating factors also should be noted.

Location - Usually, pain is described at the site of the adductor longus tendonproximally, especially with rapid adduction of the thigh. As the injury becomesmore chronic, pain may radiate distally along the medial aspect of the thighand/or proximally toward the rectus abdominis.

± Exercise-induced medial thigh pain over the area of the adductors, especially after kicking and twisting, may indicate obturator neuropathy.

± Pain at the symphysis pubis or scrotum may be more consistent with osteitis pubis. ± Conjoined tendon lesions present as pain that radiates upward into the rectus

abdominis or laterally along the inguinal ligament. Exquisite tenderness is present atthe site of the injury.



History

Quality - Acute injuries are described as a sudden ripping or stabbingpain in the groin. Chronic injuries are described as a diffuse dull ache.

Duration - Initial intense pain lasts less than a second. This initial painis soon replaced with an intense dull ache.

Severity of pain - Pain severity can vary with different patients.

Loss of function - True loss of function is not observed unless a grade3 tear is present. In the case of a severe tear, loss of hip adductionoccurs. Loss of function also should alert the physician to possiblenerve involvement (obturator nerve entrapment).

Mechanism of injury - Rapid adduction of the hip against an abductionforce (eg, changing direction suddenly in tennis), acute forced

abduction that puts an unusual stretch on the tendon (eg, a rugbytackle), and a sudden acceleration in sprinting are the most commonmechanisms of injury.



Physical

Tenderness, swelling, and ecchymosis can be observed at the superior medialthigh. Sometimes, a defect in the muscle can be palpated.

Pain is noted with resisted adduction and full passive abduction of the hip.

A pure hip adductor strain can be distinguished from combination injuriesinvolving the hip flexors (ie, iliopsoas, rectus femoris) by having the patient lie inthe supine position. If more discomfort is reproduced with resistive adductionwhen the knee and hip are extended than if the hip and knee are flexed, a purehip adductor strain can be assumed.

Physical findings can help distinguish adductor strains from other causes of groin pain such as the following:

± Iliopsoas strain - Hip flexion against resistance is painful. Tenderness is difficult to

localize because the insertion of the iliopsoas is deep. ± Osteitis pubis - Tenderness of the symphysis pubis and possible loss of full rotation of

one or both hip joints are noted.

± Conjoined tendon lesions (ie, sportsman's hernia) - Exquisite tenderness uponpalpation at the inguinal canal. Having the patient cough reproduces pain.

± Obturator neuropathy - Adductor muscle weakness, muscle spasm, and paresthesiaover the medial aspect of the distal thigh may be present. Loss of adductor tendonreflex with preservation of other muscle stretch reflexes often is observed. A positiveHowship-Romberg sign (medial knee pain induced by forced hip abduction, extension,

and internal rotation) sometimes is observed.



Management

Medical: The goals of pharmacotherapy in adductor strain areto reduce morbidity and prevent complications.

± NSAIDS ± Muscle relaxants

Surgical: Surgery is indicated in acute strains only when thereis rupture and in select chronic strains refractory toconservative treatment.

± A tenotomy for adductor longus is performed. A compressionbandage then is applied for 24 hours. The patient may walk after 2days and may resume running within pain limits 5 weekspostoperatively. The usual time period to return to unrestrictedsports activities is 10-12 weeks.



Rehabilitation

The initial management of an adductor injury should include protection, rest,ice, compression, and elevation (PRICE). Painful activities should be avoided.The use of crutches during the first few days may be indicated to relieve pain.

Some authorities believe that stretching in the acute phase may aggravate thecondition and lead to a chronic lesion. Control of muscle spasms is importantfor rehabilitation. Spasms may be alleviated with medication and/or modalities(eg, ice, electrical muscle stimulation). Passive range-of-motion (PROM)exercises are initiated when they patient can perform them without pain. Activemuscle exercises can be advanced slowly from isometric contractions withoutresistance to isometrics with resistance, progressing eventually to dynamicexercises when tolerated with little or no pain.

Strengthening abdominal and hip flexor muscles is an essential part of rehabilitation of groin injuries. Coactivation of the abdominal muscles and theadductor muscles is a useful and functional exercise. Completing manyrepetitions increases the endurance of the adductor muscles. A fatiguedmuscle/tendon complex is more vulnerable to injury. The patient should aim toprogress gradually to 30-40 repetitions. Proprioceptive exercises arerecommended, along with stretching, as well as an aquatic training program if accessible. After several days, heat and support bandages are recommended.



Grade I strain

Modalities and pain-free hip stretching exercises can begin

immediately. Pain-free progressive strengthening exercises also can be

initiated immediately and can progress to include hip flexion(with knee straight and bent) and adduction.

Therapy may be advanced to include the slide board,plyometrics (lateral sliding, lateral lunges and X lunges )and,finally, sport-specific functional drills.

The athlete may not be required to miss competition time,depending on the severity of the injury.



Grade II strain

Therapy should begin immediately with gentle pain-free activerange of motion (AROM) exercises of the hip.

Isometric exercises should be initiated as soon as the patientcan perform them without pain.

After 1 week, pain-free slide board exercises and plyometricscan be initiated.

Soon after the first week, sport-specific functional drills canbegin.

An athlete with a grade II strain may miss 3-14 days of competition, depending on the severity of the injury.



Grade III strain (nonsurgical)

PRICE plus a non ± weight-bearing restriction for acute strains

Rest for 1-3 days with continuous compression is appropriate.

If surgery is not indicated, pain-free isometric exercises and slow,pain-free AROM exercises can be started between days 3 and 5.

The athlete should continue to use crutches until normal pain-freeambulation is possible.

Initiate pain-free stretching exercises, progressive resistivestrengthening exercises (without pain), and proprioceptiveneuromuscular facilitation (PNF) between days 7 and 10.

Usually within 10 days after starting progressive resistivestrengthening exercises, the patient should be able to perform pain-free slide board exercises and plyometrics and eventually advance tosport-specific



Chronic strain

In the treatment of long-standing groin pain, rest, ice, massage, and therapeuticultrasound have been recommended. Nonsteroidal anti-inflammatory drugs(NSAIDs) and steroid injections have been suggested, but no controlled trials

have been published on the subject. Forceful adductor stretch under generalanesthetic has been recommended. A careful monitored program with a totalcessation of the sports activity is necessary for the chronic adductor injury toheal and become pain-free.

This program should consist of isometric exercises, strengthening of the hip-and pelvis-stabilizing muscles, and proprioceptive training.

± No increase in pain should be experienced during or after the exercises.

± The load of the exercises gradually is increased. Specific strengthening of the

adductor muscles then is implemented. ± Cycling can be used to maintain general conditioning. Running can begin only after the patient can perform these exercises at high intensity without pain. Sprinting andcutting activities then may follow.

± Sport-specific training is the final step before full return to sport. This part of therehabilitation program may take 3-6 months.



Hamstring strain



Hamstring injuries are common problems

that may result in significant loss of on-fieldtime for many athletes because these injuries

tend to heal slowly. Once injury occurs, the

patient is at high risk for recurrence without

proper rest and rehabilitation. While hamstring injuries can occur in people

of any age, incidence increases with age.



Aetiology

Many different causative factors can contribute to hamstringinjuries. The most significant causes include the following:

± Inadequate flexibility of the hamstrings can result in injury. Thismay be related to the patient having no or a poor stretchingroutine.

± Inadequate strength or endurance of the hamstrings with either aside-to-side weakness or an imbalance between the hamstringsand the knee extensors can lead to injury.

±M

uscle fatigue can lead to dyssynergia of muscle contraction. ± Insufficient warm-up time may be involved.

± Poor running technique may play a role.

± Return to activity before complete healing has occurred can leadto recurrence.



History

Hamstring strain is a noncontact injury and usually occurs with either acute or insidious onset. Strain injuries frequently are seen in athletes who run, jump, andkick. Avulsion injuries are seen in patients who participate in water-skiing, dancing,weight lifting, and ice-skating. The avulsion injury usually follows a burst of speed,and the patient may report a popping or tearing sensation. The most commonlyaffected muscle area in the hamstring complex is the short head of the bicepsfemoris, possibly because of its innervation.

As with most strain injuries, the injury can occur at the following 4 places: ± Origin of the muscle

± Musculotendinous junction

± Muscle belly

± Insertion of the muscle

Injury is most likely to occur while the musculotendinous junction undergoesmaximum strain during eccentric contraction of the hamstrings.

The American Medical Association (AM A) has described 3 grades of severity of hamstring injuries.

± First-degree strain is the result of stretching of the musculotendinous unit and involvestearing of only a few muscle or tendon fibers.

± Second-degree injury refers to a more severe muscle tear without complete disruption of the musculotendinous unit.

± Third-degree injury refers to a complete tear of the musculotendinous unit.



Physical

In addition to pain in the posterior thigh, the physical examination mayreveal any of the following signs or symptoms: ± Tenderness over the site of injury

± Ecchymosis

± Palpable mass A palpable defect may be felt with severe strains, but swelling and the deep

location of the muscle may obscure this finding in the acute stage.

Palpate the muscle for a defect with the patient in a prone position and the kneeflexed to 90°. This position relaxes the muscle and decreases cramping andpain. Palpate while maintaining slight tension on the muscle.

± Pain with passive extension of the knee and the hip flexed at 90°, as

compared with the noninjured side, which stretches the muscle ± Pain with resisted knee flexion, which activates the muscle



Investigations

The diagnosis is typically clinical, but some imaging studies may helpful if theclinical picture is unclear.

Radiographs can rule out an avulsion injury from the ischial tuberosity or other

fractures, but they generally are not otherwise of significant help. Ultrasonographic studies may aid the physician when confirming the diagnosis

of hamstring strain, but they do not always indicate definitive results. Thequality of the study is related to the expertise of the technician and thecooperation of the patient.

When a confirmation or grading of a hamstring strain is necessary, magneticresonance imaging (MRI) is the most sensitive test used when considering thediagnosis of hamstring strain, but it should be used sparingly because of the

cost and patient discomfort.3 Some data suggest that MRI is helpful whenattempting to predict return in a high-performance athlete in combination withsupporting clinical evidence.

Studies have shown that more than 6 weeks' delay before return to sport hasbeen reported with the following:

Complete transection Involvement of 50% of cross-sectional muscle Ganglionlike fluid collections Hemorrhagelike signal Distal myotendinous tears Deep muscle tears



Management

Medical management

±

The standard choice for medication is nonsteroidal anti-inflammatory drugs (NSAIDs). These medications not only

provide analgesia but also can decrease some of the

mediators of inflammation.

Surgical management

± Need for surgical intervention is extremely rare after ahamstring injury. Surgery is recommended only in the case

of complete rupture of the proximal or distal attachment of

the myotendinous complex into the bone.



Physical Therapy

The key to successful recovery from a hamstring

strain is recognition of the injury and of the severityof the stain.

Physical therapy (PT) is the mainstay of treatment.

The program depends on the severity of the injury

and on the time that has elapsed since the injury.

Very few scientific data are available to determinespecific rehabilitation and treatment protocols for

hamstring injuries.



Acute phase

During the acute phase (1-5 d), most of the treatment is geared towarddecreasing the inflammation and maintaining range of motion.

PRICE (ie, protection, rest, ice, compression, elevation) is the initialtreatment.

When the pain has decreased, the therapist may begin painlessgentle passive range of motion and active-assistive range of motion.

The patient also may benefit from a cane or crutches to aid inambulation to keep active.

Even if a patient with a first-degree injury is feeling better after a few

days and wants to return to participating in his or her sport, it is usuallyrecommended that he or she complete a rehabilitation program toavoid chronic injury.

Muscle strengthening, balance, and stretching should be emphasizedto the patient as a prevention of recurrence.



Subacute phase

The subacute phase (5 d to 3 wk) is when the inflammation of the injury appears to be lessening.

The goal of treatment in this stage is to begin some activerange of motion and start strengthening.

Aquatic therapy is helpful in encouraging activity withdecreased weight bearing.

Pain-free submaximal isometric exercises also are encouraged.

TENS Ice is also helpful to decrease pain and inflammation.

The patient also should resume cardiovascular training, whichmay include swimming with a pull buoy between the legs, andupper extremity exercises.



Remodeling phase

The remodeling phase (1-6 wk) is when the patient is able to perform isometricexercises at 100% effort without pain.

Prone isotonic hamstring exercises are now added to the transcutaneous

electrical nerve stimulation unit and ice. Begin unilaterally with ankle weights, using low weight and a high number of

repetitions.

Slowly increase the weight as tolerated as long as the patient's pain is notincreased afterwards.

Importantly, do not increase the weight too rapidly because this could lead to achronic injury.

Once concentric strengthening is tolerated at a normal level, the patient maybegin eccentric strengthening. Because this exercise puts the most strain onthe muscle, supervised exercising and slow progression of weight isrecommended. In the prone position, the patient performs a unilateralcontraction to 90° of knee flexion and then slowly lowers the weight.If thepatient experiences pain or stiffness, then decrease the weight to a moretolerable amount. When the affected leg is within 10% of the unaffected leg,then the patient may advance to a more aggressive therapy program.

Continued stretching of the hamstring is essential and should occur prior to

exercise. Moist heat prior to exercise may provide improved results. A posterior pelvic tilt may help eliminate lumbar compensation.



Functional stage

The functional stage is 2 weeks to 6 months.

At this point, the patient should have a normal gait pattern and canbegin fast walking. When the patient can ambulate for 20-30 minutesat a fast speed without pain or stiffness, short periods of jogging canbe added to the fast walking.

When the patient can perform a 15- to 30-minute jog, then shortperiods of sprinting may be added to the jog. Eventually, more sport-specific exercises may be added. Have the patient continue with thehamstring strengthening and stretching throughout this stage.

During the later stages of therapy, plyometric exercises may be used

to increase speed and power during training. These exercises consistof muscle stretching followed by concentric contraction, allowing for astronger contraction because of muscle facilitation and decreasedinhibition.

Low-level exercises may be used initially (eg, jumping rope), followedby higher-level exercises as tolerated (eg, side jumping over a lowobject, jumping onto and off a box). Because the higher level exercises

are associated with a higher rate of injury, they should be performedwith supervision.



Return to play

This can occur anywhere between 3 weeks and 6 months.

Isometric strength testing and flexibility testing may be

performed prior to returning to play to ensure that no subtledeficits are present that may lead to chronic injury.

The therapist must impress upon the patient the importance of stretching and warm-up prior to activities to prevent reinjury.

Less than 5 weeks are required before return to play for patients with (1) superficial muscle injury or (2) muscle injurythat involves a small cross-section of muscle.

In patients whose injury was due to poor biomechanics, careshould be taken to correct the underlying cause.

The patient should be supervised during stretching andexercise in order to assess poor technique and correct it.



Iliotibial Band Syndrome



Iliotibial band syndrome (ITBS) is the result of

inflammation and irritation of the distal portion of the iliotibial tendon as it rubs against the lateralfemoral condyle, or less commonly, the greater tuberosity.

This overuse injury occurs with repetitive flexionand extension of the knee. Inflammation andirritation of the iliotibial band (ITB) also mayoccur because of a lack of flexibility of the ITB,which can result in an increase in tension on the

ITB during the stance phase of running.



Aetiopathology

liotibial band syndrome (ITBS) typically is due to overuse. The injury isseen most commonly in runners, although other athletes (eg, cyclists,tennis players) also may be affected. The usual mechanism is irritation of

the iliotibial tract as it crosses over the lateral femoral condyle and, lesscommonly, the greater tuberosity. Increased tension or friction of the ITB inthis area can result in an increase of irritation or inflammation. Abnormalgait or running biomechanics also have been implicated.

Cyclists may experience ITBS due to improper positioning on their bike.Excessive internal or medial rotation of bike cleats and a bike seat that istoo high are 2 main causes of ITBS among cyclists.

Long-distance runners have a higher incidence of ITBS than do short-distance runners and sprinters. This higher incidence may be due to thechange in the biomechanics of running versus sprinting. Long-distancerunners tend to have a more prominent and extended heel-strike andstance phase in comparison with sprinters. The ITB is under its greatesttension during the first third of the stance phase.

Weakness of muscle groups in the kinetic chain may also result in thedevelopment of ITBS. Weakness in the hip abductor muscles, such as the

gluteus medius, may result in higher forces on the ITB and the tensor fascia lata.



Physical

The physical examination should include the entire lower extremity to rule out other causes of lateral knee or hip pain. Inmost cases, point tenderness occurs with palpation of thelateral femoral condyle or lateral tibial condyle, especially whenflexing or extending the knee, as the iliotibial band (ITB) slidesacross the lateral femoral condyle. Some patients may havetenderness over the greater trochanteric region of the hip.

Strength testing - Strength testing may reveal knee flexor or extensor weakness or hip abductor weakness.

Tests - Increased or noticeable tightness of the ITB also maybe noted upon examination with the Ober test. A modifiedThomas test can be performed to assess flexibility of the hipflexors, hamstrings, and ITB.



Management

Medical management ± NSAIDS

Surgical Intervention ± Reports of surgical intervention exist for recurrent iliotibial

band syndrome (ITBS) that has not been responsive toprevious conservative treatment.

± The operation may involve releasing the posterior portion of the ITB

performing an osteotomy of the lateral femoral epicondyle performing a bursectomy.



Physiotherapy management

Treatment for iliotibial band syndrome (ITBS) usuallyis conservative.

Conservative treatment consists of ± relative rest by decreasing the amount of exercise or

training

± the use of superficial heat and stretching prior to exercise

± the use of ice after the activity.

± Heat should be applied before and during stretching for atleast 5-10 minutes, and ice treatments should beemployed using a cold pack applied to the area for 10-15minutes or using an ice massage, which involves rubbingice over the inflamed region for 3-5 minutes or until the areais numb.



Physical therapy is one of the mainstays of treatment for ITBS,in addition to reducing the amount of inflammation and irritation.

The physical therapist can advise the athlete about waysto modify his/her training program so that faster results areseen with therapy.

Running and cycling should be decreased or avoided toprevent further repetitive stress to the ITB.

Wearing proper shoes also is very important in individuals withITBS.

Frequently, patients with ITBS demonstrate excessivepronation of their feet.

The physical therapist should evaluate the patient'sbiomechanics during walking and running and should assisthim/her in obtaining custom-made orthotics to correct faultymechanics that may be causing the ITBS.



Physical therapy treatment in the acute stage mayinclude modalities such as phonophoresis or

iontophoresis in addition to cryotherapy to decreasethe inflammation

Since some cases of ITBS are caused by excessivetension on the ITB, physical therapy can helpto incorporate proper stretching techniques into thepatient's exercise routine.

These exercises concentrate on increasing flexibilityof the ITB and of the gluteus muscles.

Other muscles that commonly need attention for flexibility include the hamstrings, quadriceps,gastrocnemius, and soleus.



This illustration demonstrates active stretching of the iliotibial band

(ITB). The athlete stands a comfortable distance from a wall and, with

the contralateral knee extended, leans the proximal shoulder against

the wall to stretch the ipsilateral ITB.



This illustration demonstrates iliotibial band syndrome stretching performed

in a side-lying position.



Soft-tissue mobilization and massage techniques may be used toassist with lengthening of the sore ITB.

Prior to mobilizing the tissues, the physical therapist may perform anultrasonographic treatment over the ITB to increase blood flow to thearea and prepare the tissues to be stretched.

Massage should generally be performed with the ITB in a lengthenedstate.

As the patient's symptoms improve, the physical therapy can progresstoward strength development and maintenance.

The physical therapist should instruct the patient in a home exerciseprogram that continues to improve the strength and endurance of thehip and knee, as well as the back and abdominals.

Strengthening of the hip abductors and knee flexors and extensors isan important component of rehabilitation.

Once the patient is able to complete all strengthening exerciseswithout discomfort, he/she may gradually return to the previoustraining regimen.



Osteitis pubis



Since 1924, osteitis pubis has been known as a noninfectious inflammation of the pubis symphysis (also known as the pubic symphysis, symphysis pubis, or symphysis pubica) causing varying degrees of lower abdominal and pelvic pain.

Osteitis pubis was first described in patients who had undergone suprapubicsurgery and remains a well-known complication of invasive procedures aboutthe pelvis.

However, it may occur as an inflammatory process in athletes.

The incidence and etiology of osteitis pubis as an inflammatory process versusan infectious process continues to fuel debate among physicians whenconfronted by a patient who presents complaining of abdominal pain or pelvicpain and overlapping symptoms.

Osteitis pubis is thought to result from inflammation of the pubis symphysisand is characterized by sclerosis and bony changes of the pubis symphysis

osteitis pubis is more prevalent in men. However, as women continue to leadmore active lifestyles, and become more involved in sports such as soccer, theincidence and prevalence of the condition may change.

Although osteitis pubis can affect all age groups, it is rarely encountered in thepediatric population. The disorder occurs most commonly in men aged 30-50years. Women are more frequently affected in their mid-30s.



Aetiology

Pregnancy/childbirth

Gynecologic surgery

Urologic surgery

Athletic activities (eg, running, football, soccer, icehockey, tennis)

Major trauma

Repeated minor trauma Rheumatologic disorders

Unknown etiology



History

Pain generally is localized over the symphysis and may radiateto the groin, medial thigh, or abdomen.

± Onset can be abrupt or insidious (more than 1 mo). ± Pain is exacerbated by activities such as running, pivoting on 1

leg, and kicking.

± Lying on one's side also may exacerbate the pain.

± Pain can occur with walking, climbing stairs, coughing, or sneezing.

The patient may experience a sensation of clicking or poppingwhen rising from a seated position, turning over in bed, or walking on uneven ground.

The patient may report weakness and difficulty ambulating.



Physical

Tenderness to palpation is noted directly

over the pubis symphysis with bilateralcompression of the greater trochanters.

The patient may report weakness, chiefly in

the hip adductors, but there also may be

involvement within the hip flexors. A waddling gait may be observed.



Imaging Studies

Plain radiographs ± Plain radiographs demonstrate sclerosis, cystic changes, or rarefaction of the medial

portions of the pubic rami (ie, marginal irregularity).

± Instability is defined as more than 2 mm of cephalad translation of the superior pubicramus on each side, with the patient standing on 1 leg in turn.

± Widening of the cleft usually is measured to greater than 10 mm.

± The sacroiliac joints also should be evaluated since laxity of one or both maycontribute to pubis symphysis instability.

± Positive findings usually are not apparent until 4 weeks after the onset of symptoms.

Bone scans may be negative but can demonstrate intense signal uptake at thepubis symphysis.

Ultrasonography may show abnormal widening of the cleft.

Computed tomography (CT) scanning is also used for evaluation of the pubissymphysis and the posterior pelvic ring.

Magnetic resonance imaging (MRI) studies may indicate bone marrow edemaat the pubis symphysis, but this finding may also be seen in asymptomaticindividuals.



Management

Medical

± NSAIDS Surgical Intervention:Different surgical

approaches have been described

± curettage

± arthrodesis

± wedge resection

± wide resection.



Physiotherapy management

Rest and time are the primary healing mechanisms.

Physical therapy (PT) may be useful during the

early stage. Modalities, such as heat or ice, mayprovide symptomatic relief. Progressive ambulationwith the aid of an assistive device (eg, cane,crutches) and possible orthoses (eg, lumbar/sacralcorset, sacroiliac belt) to unload the pelvis for painrelief and to maintain correct anatomical alignmentmay be necessary.5

Avoidance of any therapeutic exercise that mayplace stress on the pelvic ring is prudent. A homeexercise program that includes pelvic tilts may beprescribed. Experienced therapists may

attempt dynamic stabilization techniques



Congenital Coxa Vara



Coxa vara includes all forms of decrease of the femoral neck shaft angle to less than120-135°.

This condition has many etiologies: congenital, acquired, and developmental.

Congenital coxa vara (CCV), also referred to as infantile or cervical coxa vara, is acondition in which a varus deformity exists that is assumed to be caused by either anembryonic limb bud abnormality or an intrauterine condition causing significantproximal femoral varus.

CCV is, by definition, present at birth but manifests clinically during early childhoodand commonly follows a clinical course that is progressive with growth.

As a specific entity, CCV has characteristic clinical and radiographic features that helpdifferentiate it from other forms of coxa vara. It is commonly associated with a

significant limb-length discrepancy, segmental shortening of the femur, or other abnormalities of the bony femur.

Acquired forms of coxa vara are varus deformities of the proximal femur that developsecondary to metabolic, neoplastic, or traumatic conditions. This groupincludes ricketic coxa vara, fibrous dysplasia, proximal physeal injury, and prematureclosure.

Also included in this category are secondary varus changes due to generalizedskeletal conditions or dysplasias



Presentation

Patients with congenital coxa vara (CCV) usually present with gaitabnormalities. Affected children generally present between the time they begin

ambulation and age 6 years. In most patients, the gait abnormality is progressive and, notably, pain free.

Unilateral involvement with an associated relative limb-length discrepancy andTrendelenburg limp may be noted. This discrepancy in limb lengths usually ismild, ranging from 1.5 to 4.0 cm.

Patients with bilateral involvement commonly present with a waddling gaitabnormality, similar to that of patients with bilateral DDH. The Trendelenburgsign is commonly elicited in the affected hip or hips.

A tabletop examination may reveal weak abductors, a prominent greater trochanter, decreased abduction due to a decreased articulo-trochantericdistance, and coxa vara. A decrease in internal rotation also is often noted,caused by decreased femoral anteversion or true retroversion associated withthis condition.



Investigations

Radiology ± Weinstein et al proposed a

radiological means of

quantifying CCV. ± This measure, the Hilgenreiner

epiphyseal angle (HEA), is theangle subtended by thehorizontal Hilgenreiner linethrough the triradiate cartilagesand an oblique line through theproximal femoral capitalphyses, as seen in the imagebelow.

± A study of normal values of theHEA found that the angle inchildren younger than 7 yearsaverages 20°, with a widevariation of 4-35°. The meanvalue for those aged 8 years tomaturity is 23°.

Congenital coxa vara. Determination of the Hilgenreiner

epiphyseal angle, using the Hilgenreiner line as the horizontal

axis and a line through the defect adjacent to the metaphysisas the diagonal axis.



Using this measurement, patients in whom surgery is indicated includethe following: ± A child with a clinical limp and an HEA of more than 60°

± A child with a clinical limp and an HEA of 45-60° with documentedprogression of varus deformity

If left untreated, CCV historically was believed to be a relentless andprogressive deformity leading to pain and a loss of hip function withthe development of premature degenerative changes,. Some authorshave shown, however, that not all patients with the diagnosis of CCVnecessarily follow this course. On the basis of the HEA, 3 relatively

distinct groups have emerged ± In those with an HEA of less than 45°, the CCV is more commonly found tohalt progression spontaneously and to heal without intervention.

± In patients with an HEA of more than 60°, the CCV follows a moretraditional course of progressive deformity that can be aided only bysurgical intervention.

± An intermediate group with angle measurements of 45-60° represent a so-called "gray zone"; they require observation for either healing or

progression, the latter of which requires surgical intervention.



CT scan, with possible 3-dimensional

reconstructions

± anteversion or retroversion and the amount of bone stock in

the area, which is important information for preoperative

surgical planning.

MRI

±M

RI findings include widening of the growth plate withexpansion of cartilage medio-distally between the capital

femoral epiphysis and femoral metaphysis.

± The usefulness of MRI as a preoperative imaging modality,

in both diagnosis and surgical planning, is relatively limited.



Contraindications for treatment

Treatment of CCV is contraindicated inchildren who demonstrate any of thefollowing: ± Lack of symptoms on clinical assessment

± Radiographs showing an HEA of less than 45°

± Radiographs showing an HEA of 45-60° with no

documented progression

In such situations, close clinical andradiographic follow-up is warranted.



Surgical Therapy

As surgical intervention is required in a large percentage of those withcongenital coxa vara (CCV), remembering the indications for surgeryand clearly defining the goals of treatment are important to ensure the

best possible outcome and to minimize the number of surgicalprocedures for the patient.

The goals of surgical intervention are as follows:

± Correction of the neck shaft angle to a more physiologic angle and HEA toless than 35-40°

± Correction of femoral anteversion (or retroversion) to more normal values

± Ossification and healing of the defective inferomedial femoral neckfragment

± Reconstitution of the abductor mechanism through replacement of itsnormal length-tension relationship

Among the intertrochanteric osteotomies the Pauwels Y-shaped andLangenskiöld valgus-producing osteotomies have been shown toprovide good results. however, these osteotomies have a somewhatlimited ability to correct the associated femoral neck retroversion.



In early cases with mild displacement of

capital epiphysis, the epiphysis is fixed withMoore¶s pins under X-Ray control, without

attempting reduction

In cases with displacement slip is reduced by

open reduction or subtrochanteric osteotomyto change the alignment of the joint by

making epiphysis more horizontal.



Perthe¶s disease



Legg-Calve-Perthes disease (LCPD) is avascular necrosis of the proximalfemoral head resulting from compromise of the tenuous blood supply to thisarea.

LCPD usually occurs in children aged 4-10 years. The disease has an insidious onset and may occur after an injury to the hip.

In the vast majority of instances, the disorder is unilateral.

Both hips are involved in less than 10% of cases, and the joints are involvedsuccessively, not simultaneously.

It occurs more commonly in boys than in girls, with a male-to-female ratio of 4:1.

The condition is rare, occurring in approximately 4 of 100,000 children.

The cause is not known, but children with Legg-Calvé-Perthes disease (LCPD)have delayed bone age, disproportionate growth, and a mildly shortenedstature.

LCPD may be idiopathic, or it may result from a slipped capital femoralepiphysis, trauma, steroid use, sickle-cell crisis, toxic synovitis, or congenitaldislocation of the hip.



Pathophysiology

Rapid growth occurs in relation to development of the bloodsupply of the secondary ossification centers in the epiphyses,

creating an interruption of adequate blood flow and makingthese areas prone to avascular necrosis.

Interruption of the blood supply to the bone results in necrosis,removal of the necrotic tissue, and its replacement with newbone.

Bone replacement may be so complete and perfect that

completely normal bone may result. The adequacy of bone replacement depends on the age of the

patient, the presence of associated infection, congruity of theinvolved joint, and other mechanical and physiologic factors.

Necrosis may occur after trauma or infection, but idiopathiclesions can develop during periods of rapid growth of the

epiphyses.



Presentation

The earliest sign of Legg-Calvé-Perthes disease (LCPD) is an intermittent limp(abductor lurch), especially after exertion, with mild or intermittent pain in the anterior part of the thigh.

LCPD is the most common cause of a limp in the 4- to 10-year-old age group, andthe classic presentation has been described as a painless limp.

The patient may present with limited range of motion of the affected extremity.

Hip pain may develop and is a result of necrosis of the involved bone. This pain maybe referred to the medial aspect of the ipsilateral knee or to the lateral thigh.

The quadriceps muscles and adjacent thigh soft tissues may atrophy, and the hipmay develop adduction flexion contracture.

The patient may have an antalgic gait with limited hip motion.

Pain may be present with passive range of motion and limited hip movement,especially internal rotation and abduction.

Children with LCPD can have a Trendelenburg gait resulting from pain in thegluteus medius muscle.

Laboratory studies and radiography may supplement medical history taking andphysical examination in the assessment of a child with a limp.



Investigations

Obtain hip radiographs, including anteroposterior and frog-leg lateral views of the pelvis toestablish the diagnosis.

± Initial radiographs can be normal, but radiographic changes can be divided into 5 distinct stagesrepresenting a continuum of the disease process.

Stage 1 reveals cessation of femoral epiphyseal growth. Stage 2 is a subchondral fracture.

Stage 3 shows resorption.

Stage 4 demonstrates reossification.

Stage 5 is the healed or residual stage.

± Early radiographic changes may reveal only a nonspecific effusion of the joint associated with slightwidening of the joint space, metaphyseal demineralization (decreased bone density around the joint), andperiarticular swelling (bulging capsule). This is the acute phase, and it may last 1-2 weeks. Decreasingbone density in and around the joint is noted after a few weeks.

± With advancement of the disease, the joint space between the ossified head and acetabulum widens as thenecrotic ossification center appears denser than the surrounding structures. Narrowing or collapse of the

femoral head causes it to appear widened and flattened (coxa plana). A varus deformity of the femoral neckmay occur as a result of damage to the femoral head growth center and overgrowth of the greater trochanteric apophysis.

± Eventually, the disease may progress to collapse of the femoral head, increase in the width of the neck,and demineralization of the femoral head. The final shape of this area depends on the extent of necrosisand the degree of collapse. All of the findings are correlated with disease progression and the extent of necrosis. This is the active phase, and it can last 12-40 months.

A bone scan can be used to evaluate the site for avascular necrosis.



Treatment

Medical Therapy ± Consultation with an orthopedist is recommended.

± Treatment goals include eliminating hip irritability, restoring and

maintaining good range of motion in the hip, preventing femoral epiphysealcollapse, and attaining a spherical femoral head when the hip heals.

± Initial therapy includes minimal weight bearing and protection of the joint,which is accomplished by maintaining the femur abducted and internallyrotated so that the femoral head is held well inside the rounded portion of the acetabulum. Abduction and rotation of the femur is accomplished either by the use of orthotic devices (bracing) or surgery (osteotomy). TheScottish Rite brace achieves containment by abduction while allowing free

knee motion. Surgical Therapy

± Results of surgical containment appear to be better than those of nonsurgical containment (orthosis). Surgical approaches include either femoral osteotomy to redirect the involved portion within the acetabulum or innominate osteotomy. Both procedures produce equal results, but femoralosteotomy may cause shortening of the limb, leading to a chronic limp

± Surgery does not speed healing of the femoral head, but it does cause the

head to reossify in a more spherical fashion.



Irritable hip is immobilised in skin traction

As soon as spasm and pain disappear mobilise the

hip

Grade I& II no specific treatment is required

Grade III& IV when head is not deformed keep the

hip in abduction by splint or surgery (osteotomy)

Grade III& IV when head is deformed no treatment is

possible. Eventually early OA will develop which will

be treated eventualy



Physiotherapy Aims and plans

Regain max possible ROM at the affected hip alongwith strength to achieve physical independence is

the main aim ± Reduction of muscular spasm

± Isometric painless contractions

± Intermitent contraction of the hip joint

± Maintainence of the ROM

± Prevention of the contractures ± Increase of the muscular strength

± ambulation



Reduction of spasm

Primary cause if pain and deformity

Cryotherapy Moist heat

With leg in traction



Isometric painless contractions

Hip extensors

Abductors quads



Intermitent contraction of the hip joint

Early slow relaxed passive movements

Helps in maintaining nutrition Helps in maintaining length of soft tissues



Maintainence of the ROM

Full ROM of hip

Extension, abduction &IR to be carried out atregular intervals and recorded

Splint if resting position is not corrected



Prevention of the contractures

Flexor tightness and contracture is common

Gait affected Gentle extension of affected and stretching of

Normal

Wieght can be added to maintain

Prone lying



Increase of the muscular strength

After pain and spasm decrease

Active assisted, assisted resisted & resisted Terminal ranges of Abduction and extension,

quads&hams and dorsiflexors and

plantarflexors



ambulation

POP or abduction splint no wt bearing hence

parallel bar non wt bearing and standing Walker then crutches



POE

Scottish rite brace



Petrie plaster method/broomstick

Hip in 30 abduction and 20 internal rotationwith 15 flexion in knee

Active mobilisaton initiated after removal

Starting from relaxed passive movements to

resisted



P T management following surgery

(varus derotation osteotomy)

Limb is immobilized in hip spica for 6wks

Toe movements Isometrics for knee and hip inside plaster

Resisted movm of contra lateral

After removal relaxed passive movements

manually then CPM

Mobilisation, strengthening then gait training



Avascular necrosis (AVN/ Osteonecrosis)



Osteonecrosis of the femoral head involves the hip joint, withosteocytes of the femoral head dying along with the bone marrow;resorption of the dead tissue by new but weaker osseous tissue can

then lead to subchondral fracture and collapse. There are 2 forms of osteonecrosis:

± traumatic (the most common form)

± atraumatic.

Other terms to describe this disorder are avascular necrosis andischemic necrosis to denote vascular etiology.

The term aseptic necrosis also has been used to indicate that infection

does not play a causative role. Alexander Munro first identified the condition in 1738. In the mid

1800s, Cruveilhier was the first to attribute the disorder to anaberration of circulation in the femoral head. Diagnosis of this disorder has increased because of improved technology and increasedawareness.



Aetiology

As the name implies, traumatic osteonecrosis is secondary todirect injury to the femoral head with resultant damage of theblood supply. Fracture of the femoral head or neck and hip

dislocation are the primary mechanisms of injury. Atraumatic osteonecrosis has many risk factors. The most

commonly associated problems are corticosteroid use andalcohol abuse. Other factors includesickle cell anemia, Gaucher disease, systemic lupus erythematosus, coagulopathies,hyperlipidemia, organ transplantation, caisson disease, andthyroid disorders. Genetic factors may also play a role

The idiopathic cases make up the third most common category.

Hip osteonecrosis resulting from corticosteroid use or alcoholabuse is associated with the worst prognosis.



X-rays ± Anteroposterior (AP) radiographs and frog lateral radiographs of

both hips are the primary diagnostic modalities.

MRI ± Sensitivity and specificity is greater than 98%, which is higher than

all other modalities.

± This study is ideal if x-ray findings are normal and clinicalsuspicion is high. MRI should be performed in all patients withosteonecrosis to assess the extent of the disease. Three-dimensionalMRI scanning with image registration may be used to

assess changes in lesion size. ± MRI is recommended to identify bilateral disease when 1 hip has

radiographic signs of disease and the other is normal (see imagebelow).



International classification of osteonecrosisof the femoral head (Association ResearchCirculation Osseus [ARCO])

Stage 0 - Bone biopsy results consistent with osteonecrosis; other test results normal

Stage I - Positive findings on bone scan,MRI, or both ± A - <15% involvement of the femoral head (MRI)

± B - 15-30% involvement ± C - >30% involvement

Stage II - Mottled appearance of femoral head, osteosclerosis, cyst formation, andosteopenia on radiographs; no signs of collapse of femoral head on radiographic or CT study; positive findings on bone scan and MRI; no changes in acetabulum

± A - <15% involvement of the femoral head (MRI)

± B - 15-30% involvement

± C - >30% involvement

Stage III - Presence of crescent sign lesions classified on basis of appearance on APand lateral radiographs ± A - <15% crescent sign or <2-mm depression of femoral head

± B - 15-30% crescent sign or 2- to 4-mm depression

± C - >30% crescent sign or >4-mm depression

Stage IV - Articular surface flattened; joint space shows narrowing; changes inacetabulum with evidence of osteosclerosis, cyst formation, and marginal osteophytes



Medical Management

Nonsurgical treatment of osteonecrosis is limited. Observation andprotected weight bearing are options. Certain cases of early-stagedisease can be treated successfully with this option. However, most

studies indicate that the risk of disease progression is greater withnonsurgical treatment than with surgical intervention.

Nonsteroidal anti-inflammatory drugs can be used to reduce pain andinflammation in patients who cannot have surgery for medical or other reasons or for patients who are undergoing surgical treatment.

Physical therapy can be helpful to restore motion and improve gait.

Electrical stimulation has been used in several centers. In some

studies, it has been helpful in treatment prior to femoral head collapse.



Surgical Therapy

The mainstay of treatment for osteonecrosis

is surgical. Numerous procedures are

available, indicating that no single procedure

is distinctly advantageous. Preoperative

staging, particularly with collapse of the

femoral head, and acetabular involvementare the determining factors for choosing a

particular operation.

conditions in and around the hip joint

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