The diagnosis is a combination of clinical suspicion plus radiological investigation. Children with a SCFE experience a decrease in their range of motion, and are often unable to complete hip flexion or fully rotate the hip inward. 20-50% of SCFE are missed or misdiagnosed on their first presentation to a medical facility. SCFEs may be initially overlooked, because the first symptom is knee pain, referred from the hip. The knee is investigated and found to be normal.

The diagnosis requires x-rays of the pelvis, with anteriorposterior (AP) and frog-leg lateral views. The appearance of the head of the femur in relation to the shaft likens that of a "melting ice cream cone", visible with Klein's line. The severity of the disease can be measured using the Southwick angle.

Most countries have standard newborn exams that include a hip joint exam screening for early detection of hip dysplasia.

Sometimes during an exam a "click" or more precisely "clunk" in the hip may be detected (although not all clicks indicate hip dysplasia). When a hip click (also known as "clicky hips" in the UK) is detected, the child's hips are tracked with additional screenings to determine if developmental dysplasia of the hip is caused.

Two maneuvers commonly employed for diagnosis in neonatal exams are the Ortolani maneuver and the Barlow maneuver.

In order to do the Ortolani maneuver it is recommended that the examiner put the newborn baby in a position in which the contralateral hip is held still while the thigh of the hip being tested is abducted and gently pulled anteriorly. If a "clunk" is heard (the sound of the femoral head moving over the acetabulum), the joint is normal, but absence of the "clunk" sound indicates that the acetabulum is not fully developed. The next method that can be used is called the Barlow maneuver. It is done by adducting the hip while pushing the thigh posteriorly. If the hip goes out of the socket it means it is dislocated, and the newborn has a congenital hip dislocation. The baby is laid on its back for examination by separation of its legs. If a clicking sound can be heard, it indicates that the baby may have a dislocated hip. It is highly recommended that these maneuvers be done when the baby is not fussing, because the baby may inhibit hip movement.

The condition can be confirmed by ultrasound and X-ray. Ultrasound imaging yields better results defining the anatomy until the cartilage is ossified. When the infant is around 3 months old a clear roentgenographic image can be achieved. Unfortunately the time the joint gives a good x-ray image is also the point at which nonsurgical treatment methods cease to give good results. In x-ray imaging dislocation may be indicated if the Shenton's line (an arc drawn from the medial aspect of the femoral neck through the superior margin of the obturator foramen) does not result in a smooth arc. However, in infants this line can be unreliable as it depends on the rotation of the hip when the image is taken ()

Asymmetrical gluteal folds and an apparent limb-length inequality can further indicate unilateral hip dysplasia. Most vexingly, many newborn hips show a certain ligamentous laxity, on the other hand severely malformed joints can appear stable. That is one reason why follow-up exams and developmental monitoring are important. Frequency and methods of routine screenings in children is still in debate however physical examination of newborns followed by appropriate use of hip ultrasound is widely accepted.

The Harris hip score (developed by William H. Harris MD, an orthopedist from Massachusetts) is one way to evaluate hip function following surgery. Other scoring methods are based on patients' evaluation like e.g. the Oxford hip score, HOOS and WOMAC score. Children's Hospital Oakland Hip Evaluation Scale (CHOHES) is a modification of the Harris hip score that is currently being evaluated.

Hip dysplasia can develop in older age. Adolescents and adults with hip dysplasia may present with hip pain and in some cases hip labral tears. X-rays are used to confirm a diagnosis of hip dysplasia. CT scans and MRI scans are occasionally used too.

X-rays of the hip may suggest and/or verify the diagnosis. X-rays usually demonstrate a flattened, and later fragmented, femoral head. A bone scan or MRI may be useful in making the diagnosis in those cases where X-rays are inconclusive. Usually, plain radiographic changes are delayed 6 weeks or more from clinical onset, so bone scintigraphy and MRI are done for early diagnosis. MRI results are more accurate, i.e. 97 to 99% against 88 to 93% in plain radiography. If MRI or bone scans are necessary, a positive diagnosis relies upon patchy areas of vascularity to the capital femoral epiphysis (the developing femoral head).

Some sources prefer "developmental dysplasia of the hip" (DDH) to "congenital dislocation of the hip" (CDH), finding the latter term insufficiently flexible in describing the diversity of potential complications.

The use of the word congenital can also imply that the condition already exists at birth. This terminology introduces challenges, because the joint in a newborn is formed from cartilage and is still malleable, making the onset difficult to ascertain.

The newer term DDH also encompasses occult dysplasia (e.g. an underdeveloped joint) without dislocation and a dislocation developing after the "newborn" phase.

The term is not used consistently. In pediatric/neonatal orthopedics it is used to describe unstable/dislocatable hips and poorly developed acetabula. For adults it describes hips showing abnormal femur head or acetabular x-rays.

Some sources prefer the term "hip dysplasia" over DDH, considering it to be "simpler and more accurate", partly because of the redundancy created by the use of the terms developmental and dysplasia. Types of DDH include subluxation, dysplasia, and dislocation. The main types are the result of either laxity of the supporting capsule or an abnormal acetabulum.

Presence at birth is extremely rare and associated with other congenital anomalies such as proximal femoral focal deficiency, fibular hemimelia or anomalies in other part of the body such as cleidocranial dyastosis. The femoral deformity is present in the subtrochantric area where the bone is bent. The cortices are thickened and may be associated with overlying skin dimples. External rotation of the femur with valgus deformity of knee may be noted. This condition does not resolve and requires surgical management. Surgical management includes valgus osteotomy to improve hip biomechanics and length and rotational osteotomy to correct retroversion and lengthening.

The disease can be treated with external in-situ pinning or open reduction and pinning. Consultation with an orthopaedic surgeon is necessary to repair this problem. Pinning the unaffected side prophylactically is not recommended for most patients, but may be appropriate if a second SCFE is very likely.

Once SCFE is suspected, the patient should be non-weight bearing and remain on strict bed rest. In severe cases, after enough rest the patient may require physical therapy to regain strength and movement back to the leg. A SCFE is an orthopaedic emergency, as further slippage may result in occlusion of the blood supply and avascular necrosis (risk of 25 percent). Almost all cases require surgery, which usually involves the placement of one or two pins into the femoral head to prevent further slippage. The recommended screw placement is in the center of the epiphysis and perpendicular to the physis. Chances of a slippage occurring in the other hip are 20 percent within 18 months of diagnosis of the first slippage and consequently the opposite unaffected femur may also require pinning.

The risk of reducing this fracture includes the disruption of the blood supply to the bone. It has been shown in the past that attempts to correct the slippage by moving the head back into its correct position can cause the bone to die. Therefore the head of the femur is usually pinned 'as is'. A small incision is made in the outer side of the upper thigh and metal pins are placed through the femoral neck and into the head of the femur. A dressing covers the wound.

Children younger than 6 have the best prognosis, since they have time for the dead bone to revascularize and remodel, with a good chance that the femoral head will recover and remain spherical after resolution of the disease. Children who have been diagnosed with Perthes' disease after the age of 10 are at a very high risk of developing osteoarthritis and coxa magna. When an LCP disease diagnosis occurs after age 8, a better outcome results with surgery rather than nonoperative treatments. Shape of femoral head at the time when Legg-Calve Perthes disease heals is the most important determinant of risk for degenerative arthritis; hence, the shape of femoral head and congruence of hip are most useful outcome measures.

More common cause: primary defect in endochondral ossification of the medial part of the femoral neck.

Excessive interuterine pressure on the developing fetal hip.

vascular insult.

Faulty maturation of the cartilage and metaphyseal bone of the femoral neck.

Clinical feature: presents after the child has started walking but before six years of age. Usually associated with a painless hip due to mild abductor weakness and mild limb length discrepancy.

If there is a bilateral involvement the child might have a waddling gait or trendelenburg gait with an increased lumbar lordosis. The greater trochanter is usually prominent on palpation and is more proximal. Restricted abduction and internal rotation.

X-ray: decreased neck shaft angle, increased cervicofemoral angle, vertical physis, shortened femoral neck decrease in femoral anteversion. HE angle (hilgenriener epiphyseal angle- angle subtended between a horizontal line connecting the triradiate cartilage and the epiphysisn normal angle is <30 degrees.

Treatment:

HE angle of 45–60 degrees observation and periodic follow up.

Indication for surgery :HE angle more than 60 degrees, progressive deformity, neckshaft angle <90 degrees, development of trendelenburg gait

Surgery: subtrochantric valgus osteotomy with adequate internal rotation of distal fragment to correct anteversion

common complication is recurrence. If HE angle is reduced to 38 degrees less evidence of recurrence

post operative spica cast is used for a period of 6–8 weeks.

Coxa vara is also seen in Niemann–Pick disease.

Different features of the dysostosis are significant. Radiological imaging helps confirm the diagnosis. During gestation (pregnancy), clavicular size can be calculated using available nomograms. Wormian bones can sometimes be observed in the skull.

Diagnosis of CCD spectrum disorder is established in an individual with typical clinical and radiographic findings and/or by the identification of a heterozygous pathogenic variant in RUNX2 (CBFA1).

Exact diagnosis remains widely built on precise history taking, with the characteristic clinical and radiographic skeletal features. Genetic diagnosis is based on DNA sequencing. Because plasma COMP levels are significantly reduced in patients with COMP mutations, such as pseudoachondroplasia, measuring plasma COMP levels has become a reliable means of diagnosing this and pathopysiologically similar disorders.

Coxa valga is a deformity of the hip where the angle formed between the head and neck of the femur and its shaft is increased, usually above 135 degrees. It is caused by a slipped epiphysis of the femoral head.

The differential diagnosis includes neuromuscular disorders (i.e. cerebral palsy, spinal dysraphism, poliomyelitis), skeletal dysplasias, and juvenile idiopathic arthritis.

There are no set standards for the diagnosis of suspected transient synovitis, so the amount of investigations will depend on the need to exclude other, more serious diseases.

Inflammatory parameters in the blood may be slightly raised (these include erythrocyte sedimentation rate, C-reactive protein and white blood cell count), but raised inflammatory markers are strong predictors of other more serious conditions such as septic arthritis.

X-ray imaging of the hip is most often unremarkable. Subtle radiographic signs include an accentuated pericapsular shadow, widening of the medial joint space, lateral displacement of the femoral epiphyses with surface flattening (Waldenström sign), prominent obturator shadow, diminution of soft tissue planes around the hip joint or slight demineralisation of the proximal femur. The main reason for radiographic examination is to exclude bony lesions such as occult fractures, slipped upper femoral epiphysis or bone tumours (such as osteoid osteoma). An anteroposterior and frog lateral (Lauenstein) view of the pelvis and both hips is advisable.

An ultrasound scan of the hip can easily demonstrate fluid inside the joint capsule (Fabella sign), although this is not always present in transient synovitis. However, it cannot reliably distinguish between septic arthritis and transient synovitis. If septic arthritis needs to be ruled out, needle aspiration of the fluid can be performed under ultrasound guidance. In transient synovitis, the joint fluid will be clear. In septic arthritis, there will be pus in the joint, which can be sent for bacterial culture and antibiotic sensitivity testing.

More advanced imaging techniques can be used if the clinical picture is unclear; the exact role of different imaging modalities remains uncertain. Some studies have demonstrated findings on magnetic resonance imaging (MRI scan) that can differentiate between septic arthritis and transient synovitis (for example, signal intensity of adjacent bone marrow). Skeletal scintigraphy can be entirely normal in transient synovitis, and scintigraphic findings do not distinguish transient synovitis from other joint conditions in children. CT scanning does not appear helpful.

Accurate assessment of plain radiographic findings remains an important contributor to diagnosis of pseudoachondroplasia. It is noteworthy that vertebral radiographic abnormalities tend to resolve over time. Epiphyseal abnormalities tend to run a progressive course. Patients usually suffer early-onset arthritis of hips and knees. Many unique skeletal radiographic abnormalities of patients with pseudoachondroplasia have been reported in the literature.

- Together with rhizomelic limb shortening, the presence of epiphyseal-metaphyseal changes of the long bones is a distinctive radiologic feature of pseudoachondroplasia.

- Hypoplastic capital femoral epiphyses, broad short femoral necks, coxa vara, horizontality of acetabular roof and delayed eruption of secondary ossification center of os pubis and greater trochanter.

- Dysplastic/hypoplastic epiphyses especially of shoulders and around the knees.

- Metaphyseal broadening, irregularity and metaphyseal line of ossification. These abnormalities that are typically encountered in proximal humerus and around the knees are collectively known as “rachitic-like changes”.

- Radiographic lesions of the appendicular skeleton are typically bilateral and symmetric.

- Oval shaped vertebrae with anterior beak originating and platyspondyly demonstrated on lateral radiographs of the spine.

- Normal widening of the interpedicular distances caudally demonstrated on anteroposterior radiographs of the dorsolumbar region. This is an important differentiating feature between pseudoachondroplasia and achondroplasia.

- Odontoid hypoplasia may occur resulting in cervical instability.

Pain in or around the hip and/or limp in children can be due to a large number of conditions. Septic arthritis (a bacterial infection of the joint) is the most important differential diagnosis, because it can quickly cause irreversible damage to the hip joint. Fever, raised inflammatory markers on blood tests and severe symptoms (inability to bear weight, pronounced muscle guarding) all point to septic arthritis, but a high index of suspicion remains necessary even if these are not present. Osteomyelitis (infection of the bone tissue) can also cause pain and limp.

Bone fractures, such as a toddler's fracture (spiral fracture of the shin bone), can also cause pain and limp, but are uncommon around the hip joint. Soft tissue injuries can be evident when bruises are present. Muscle or ligament injuries can be contracted during heavy physical activity —however, it is important not to miss a slipped upper femoral epiphysis. Avascular necrosis of the femoral head (Legg-Calvé-Perthes disease) typically occurs in children aged 4–8, and is also more common in boys. There may be an effusion on ultrasound, similar to transient synovitis.

Neurological conditions can also present with a limp. If developmental dysplasia of the hip is missed early in life, it can come to attention later in this way. Pain in the groin can also be caused by diseases of the organs in the abdomen (such as a psoas abscess) or by testicular disease. Rarely, there is an underlying rheumatic condition (juvenile idiopathic arthritis, Lyme arthritis, gonococcal arthritis, ...) or bone tumour.

Around 5 years of age, surgical correction may be necessary to prevent any worsening of the deformity. If the mother has dysplasia, caesarian delivery may be necessary. Craniofacial surgery may be necessary to correct skull defects. Coxa vara is treated by corrective femoral osteotomies. If there is brachial plexus irritation with pain and numbness, excision of the clavicular fragments can be performed to decompress it. In case of open fontanelle, appropriate headgear may be advised by the orthopedist for protection from injury.

This condition is usually curable with appropriate treatment, or sometimes it heals spontaneously. If it is painless, there is little cause for concern.

Correcting any contributing biomechanical abnormalities and stretching tightened muscles, such as the iliopsoas muscle or iliotibial band, is the goal of treatment to prevent recurrence.

Referral to an appropriate professional for an accurate diagnosis is necessary if self treatment is not successful or the injury is interfering with normal activities. Medical treatment of the condition requires determination of the underlying pathology and tailoring therapy to the cause. The examiner may check muscle-tendon length and strength, perform joint mobility testing, and palpate the affected hip over the greater trochanter for lateral symptoms during an activity such as walking.

A self-treatment recommended by the U.S. Army for a soft tissue injury of the iliopsoas muscle treatment, like for other soft tissue injuries, is a HI-RICE (Hydration, Ibuprofen, Rest, Ice, Compression, Elevation) regimen lasting for at least 48 to 72 hours after the onset of pain. "Rest" includes such commonsense prescriptions as avoiding running or hiking (especially on hills), and avoiding exercises such as jumping jacks, sit-ups or leg lifts/flutter kicks.

Stretching of the tight structures (piriformis, hip abductor, and hip flexor muscle) may alleviate the symptoms. The involved muscle is stretched (for 30 seconds), repeated three times separated by 30 second to 1 minute rest periods, in sets performed two times daily for six to eight weeks. This should allow one to progress back into jogging until symptoms disappear.

Spondyloepiphyseal dysplasia congenita (abbreviated to SED more often than SDC) is a rare disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and occasionally problems with vision and hearing. The name of the condition indicates that it affects the bones of the spine (spondylo-) and the ends of bones (epiphyses), and that it is present from birth (congenital). The signs and symptoms of spondyloepiphyseal dysplasia congenita are similar to, but milder than, the related skeletal disorders achondrogenesis type 2 and hypochondrogenesis. Spondyloepiphyseal dysplasia congenita is a subtype of collagenopathy, types II and XI.

Radiographic features include delayed epiphyseal ossification at the hips and knees, platyspondyly with irregular end plates and narrowed joint spaces, diffuse early osteoarthritic changes (in the spine and hands), mild brachydactyly and mild metaphyseal abnormalities which predominantly involve the hips and knees.

Spondyloepimetaphyseal dysplasia, Strudwick type is an inherited disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and problems with vision. The name of the condition indicates that it affects the bones of the spine (spondylo-) and two regions near the ends of bones (epiphyses and metaphyses). This type was named after the first reported patient with the disorder. Spondyloepimetaphyseal dysplasia, Strudwick type is a subtype of collagenopathy, types II and XI.

The signs and symptoms of this condition at birth are very similar to those of spondyloepiphyseal dysplasia congenita, a related skeletal disorder. Beginning in childhood, the two conditions can be distinguished in X-ray images by changes in areas near the ends of bones (metaphyses). These changes are characteristic of spondyloepimetaphyseal dysplasia, Strudwick type.

Spondyloepimetaphyseal dysplasia, Pakistani type is a form of spondyloepimetaphyseal dysplasia involving "PAPSS2" (also known as "ATPSK2"). The condition is rare.

People with spondyloepiphyseal dysplasia are short-statured from birth, with a very short trunk and neck and shortened limbs. Their hands and feet, however, are usually average-sized. This type of dwarfism is characterized by a normal spinal column length relative to the femur bone. Adult height ranges from 0.9 meters (35 inches) to just over 1.4 meters (55 inches). Curvature of the spine (kyphoscoliosis and lordosis) progresses during childhood and can cause problems with breathing. Changes in the spinal bones (vertebrae) in the neck may also increase the risk of spinal cord damage. Other skeletal signs include flattened vertebrae (platyspondyly), a hip joint deformity in which the upper leg bones turn inward (coxa vara), and an inward- and downward-turning foot (called clubfoot). Decreased joint mobility and arthritis often develop early in life. Medical texts often state a mild and variable change to facial features, including cheekbones close to the nose appearing flattened, although this appears to be unfounded. Some infants are born with an opening in the roof of the mouth, which is called a cleft palate. Severe nearsightedness (high myopia) is sometimes present, as are other eye problems that can affect vision such as detached retinas. About one-quarter of people with this condition have mild to moderate hearing loss.

People with this condition are short-statured from birth, with a very short trunk and shortened limbs. Their hands and feet, however, are usually average-sized. Curvature of the spine (scoliosis and lumbar lordosis) may be severe and can cause problems with breathing. Changes in the spinal bones (vertebrae) in the neck may also increase the risk of spinal cord damage. Other skeletal signs include flattened vertebrae (platyspondyly), severe protrusion of the breastbone (pectus carinatum), a hip joint deformity in which the upper leg bones turn inward (coxa vara), and a foot deformity known as clubfoot.

Affected individuals have mild and variable changes in their facial features. The cheekbones close to the nose may appear flattened. Some infants are born with an opening in the roof of the mouth, which is called a cleft palate. Severe nearsightedness (high myopia) and detachment of the retina (the part of the eye that detects light and color) are also common.

Clinical:

Patients often present with a history of fever of unknown origin, muscular weakness, poor development, abnormal dentition, normal serum calcium, phosphorus, and alkaline phosphatase levels. Associated clinical findings also include glaucoma, photosensitivity, heart block, foot deformities, and chronic psoriasiform skin lesions.

Radiological:

Classic radiologic findings were first described by Edward B. Singleton and David Merten in 1973.

Typical radiographic appearances include skeletal demineralization, expanded shafts of the metacarpals and phalanges with widenend medullary cavities, cardiomegaly, and intramural calcification of the proximal aorta with occasional extension into the aortic or mitral valves.

Other commonly seen radiographic findings include shallow acetabular fossa, subluxation of the femoral head, coxa valga, hypoplastic radial epiphysis, soft tissue calcifications between the radius and ulna, constriction of the proximal radial shaft, acro-osteolysis, and equinovarus foot deformities.

Singleton Merten Syndrome is an autosomal dominate genetic disorder with variable expression with an onset of symptoms during childhood.