Dislocation of hip

• A dislocated hip is a condition that can be congenital or acquired.

• Congenital hip dislocations are much more common in girls than in boys.

• Congenital hip dislocation: The abnormal formation of the hip joint in which the ball at the top of the thighbone (the femoral head) is not stable within the socket (the acetabulum). The ligaments of the hip joint may also be loose and stretched.

• The degree of instability or looseness varies. A baby born with this condition may have the ball of the hip loosely in the socket (subluxed) or the ball of the hip may be completely dislocated at birth.

• Untreated, the condition may cause legs of different lengths and a "duck-like" walk and lead to pain on walking and early osteoarthritis.

• One of the early signs that a baby has been born with a dislocated hip may be a;

- clicking sound when the baby's legs are moved apart.

-With a full dislocation, the leg "rides up" so it is shorter than its mate.

-The buttocks folds also may not be symmetrical with more creases on the dislocated side..

• treatment is a device called the Pavlik harness, which has straps that allow the baby to move about freely while holding the hip in place and preventing movements

• In most up to 97% of cases, the Pavlik harness is effective. If it is not, the hip may be positioned into place under anesthesia (closed reduction) and maintained with a body cast (a spica).

• Congenital hip dislocation is also known as developmental dislocation or dysplasia.

Types of misalignments of femur head to socket in hip dysplasia. A:

Normal. B: Dysplasia. C: Subluxation. D: Luxation

Posterior vs. anterior

• Nine out of ten hip dislocations are posterior. The affected limb will be shortened and internally rotated in this case.

• In an anterior dislocation the limb will not be lengthened as noticeably and will be externally rotated.

Diagnostics

• Physical Examination

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

• The condition can be confirmed by ultrasound and X-ray

• Congenital hip dislocation must be detected early when it can be easily treated by a few weeks of traction.

• If it is not detected, the child's hip may develop incorrectly seen when the child begins to walk.

Causes

• Some studies suggest a hormonal link Specifically the hormone relaxin has been indicated

• A genetic factor is indicated by the trait running in families and increased occurrence in some ethnic population

• If one hip is affected the child will have a limp and lurch and with bilateral dislocation there will be a waddling gait.

• On physical exam, with the baby in the supine position, the examiner flexes the hips and knees both to 90 degrees, and, holding the knees, pushes gently downward, which may induce a posterior dislocation or subluxation. Keeping the baby in this 90 degree flexed position, the examiner then externally rotates the thighs. A normal infant will demonstrate no evidence of dislocation. It can also be detected with the Galeazzi test.

• The Galeazzi test is used in the assessment of congenital dislocation/developmental dysplasia of the hip. It is performed by flexing an infant's knees in the supine position so that the ankles touch the buttocks. If the knees are not level then the test is positive, indicating a potential congenital hip malformation

Acquired hip dislocations

• Acquired hip dislocations are extremely painful and commonly occur during car accidents. They may be treated by surgical realignment and traction.

Acquired

• risk factors include breech birth and firstborns.In breech position the femoral head tends to get pushed out of the socket. A narrow uterus also facilitates hip joint dislocation during fetal development and birth.

Treatment

• Early hip dysplasia can often be treated using a Pavlik harness (see photograph) or the Frejka pillow/splint in the first year of life with usually normal results.

• Other devices employed include the spica cast, particularly following surgical closed reduction. A few weeks in traction can be used as part of a treatment plan.

baby wearing a Pavlik harness

Diagram of Pavlik harness

Diagram of Frejka pillow

Traction

talipes

• Definition

• Clubfoot is a condition in which one or both feet are twisted into an abnormal position at birth. The condition is also known as talipes. Read more: Clubfoot - symptoms, stages, Definition, Description, Demographics, Causes and symptoms, Diagnosis, Treatment, Prognosis, Prevention http://www.healthofchildren.com/C/Clubfoot.html#ixzz0b2ODqaRe

• True clubfoot is usually obvious at birth because a clubfoot has a typical appearance of pointing downward and being twisted inwards. Since the condition starts in the first trimester of pregnancy, the abnormality is quite well established at birth, and the foot is often very rigid. Uncorrected clubfoot in an adult causes only part of the foot, usually the outer edge or the heel or the toes, to touch the ground. For a person with clubfoot, walking becomes difficult or impossible.

• True clubfoot is characterized by abnormal bone formation in the foot.

• There are four variations of clubfoot: 1) talipes varus, - clubfoot, the foot generally turns inward

so that the leg and foot look somewhat like the letter J (when looking at the left foot head-on).

2) talipes valgus, - the foot rotates outward like the letter L. 3) talipes equines, - the foot points downward, similar to

that of a toe dancer. 4) talipes calcaneus - the foot points upward, with the heel

pointing down.

Demographics

• The ratio of males to females with clubfoot is 2.5 to 1

• In the United States, the incidence is approximately one in every 1,000 live births.

• A family history of clubfoot has been reported in 24.4 percent of families in a single study. These findings suggest the potential role of one or more genes being responsible for clubfoot. Read more:

Causes and symptoms

• Several environmental causes have been proposed for clubfoot. Many obstetricians feel that intrauterine crowding causes clubfoot. This theory is supported by a significantly higher incidence of clubfoot among twins compared to singleton births. Intrauterine exposure to the drug misoprostol has been linked with clubfoot. Misoprostol is commonly used when trying, usually unsuccessfully, to induce abortion in Brazil and in other countries in South and Central America. Researchers in Norway have reported that males who are in the printing trades have significantly more offspring with clubfoot than men in other occupations. For unknown reasons, amniocentesis , a prenatal test, has also been associated with clubfoot. The infants of mothers who smoke during pregnancy have a greater chance of being born with clubfoot than are offspring of women who do not smoke.

•

• The physical appearance of a clubfoot may vary. However, at birth, an affected foot usually turns inward and points downward. It resists realignment. The calf muscle may be smaller and less well developed than normal. One or both feet may be affected.

Diagnosis

• Clubfoot is diagnosed by physician inspection. This is most often completed immediately after birth. Clubfoot may be suspected during the latter stages of pregnancy, especially in a mother of shorter or smaller than normal stature, a large fetus, or multiple infants.

Treatment

• Clubfoot is corrected by casting or surgery. To have the best chances for successful resolution without resorting to surgery, treatment as soon after birth as possible. The Ponseti method of stretching and casting has been used with increasing success since the 1990s. The Ponseti method requires that a doctor stretch the child's affected foot toward its anatomically correct position and hold it in place with a cast. The foot is realigned and a new cast applied weekly for several weeks. Once the correct position has been achieved, a brace must be worn during periods of sleep to maintain the correction. To be successful, the method requires active parental involvement.

Treatment

• When casting and bracing are not successful, surgery may be required to realign the tendons, ligaments, and joints in the foot and ankle. Such a procedure is usually completed between nine and 12 months of age. After surgery, a cast holds the foot in the desired position.

prognosis

• The prognosis for successfully treating clubfoot is good at this time. Persons with clubfoot that is corrected by surgery may notice some increased stiffness in their affected feet as they age. A corrected clubfoot is often a shoe size smaller than normal and may be somewhat less flexible. The calf muscles in an affected clubfoot leg may be slightly smaller than an unaffected leg. However, without treatment, clubfoot will result in a functional disability.

Parental concerns

• Parents of an infant with clubfoot should be prepared to participate in treatment for two or more years. They should seek prompt treatment from a qualified health care provider.

• Talipes (tal´ĭ-pēz)   a deformity in which the foot is twisted out of normal position; see also clubfoot. It may have an abnormally high longitudinal arch (talipes cavus) or it may be in dorsiflexion (talipes calcaneus), in plantar flexion (talipes equinus), abducted and everted (talipes valgus or flatfoot), adducted and inverted (talipes varus), or various combinations of these (talipes calcaneovalgus, talipes calcaneovarus, talipes equinovalgus, or talipes equinovarus).

Congenital talipes equinovarus (CTEV), often known as 'clubfoot', is a poorly understood but common developmental disorder of the lower

limb,

Osteogenesis Imperfecta

• Osteogenesis imperfecta (OI) is a genetic disorder in which bones break easily. Sometimes the bones break for no known reason. OI can also cause weak muscles, brittle teeth, a curved spine and hearing loss. The cause is a gene defect that affects how you make collagen, a protein that helps make bones strong. Usually you inherit the faulty gene from a parent. Sometimes, it is due to a mutation, a random gene change.

• OI can range from mild to severe and symptoms vary from person to person. A person may have just a few or as many as several hundred fractures in a lifetime. There is no cure, but you can manage symptoms. Treatments include exercise, pain medicine, physical therapy, wheelchairs, braces and surgery.

• Osteogenesis imperfecta (OI) is a genetic disorder characterized by bones that break easily, often from little or no apparent cause. A classification system of different types of OI is commonly used to help describe how severely a person with OI is affected. For example, a person may have just a few or as many as several hundred fractures in a lifetime.

• Prevalence

• Although the number of people affected with OI in the United States is unknown, the best estimate suggests a minimum of 20,000 and possibly as many as 50,000.

• Diagnosis• OI is caused by genetic defects that affect the body’s ability to make

strong bones. Collagen is the major protein of the body’s connective tissue and can be likened to the framework around which a building is constructed. In dominant (classical) OI, a person has either too little type 1 collagen or a poor quality of type 1 collagen caused by a mutation in one of the type 1collagen genes. In recessive OI, mutations in other genes interfere with collagen production. The result in all cases is weak bones that break easily.

• It is often possible to diagnose OI based solely on clinical features. Clinical geneticists can perform biochemical (collagen) or molecular (DNA) tests that can help confirm a diagnosis of OI in some situations.

• These tests generally require several weeks before results are known. Both the collagen biopsy test and the DNA test are thought to detect nearly 90 percent of all type 1collagen mutations.

• Clinical Features• The characteristic features of OI vary greatly from person to person,

even among people with the same type of OI and even within the same family. Not all characteristics are evident in each case. The majority of OI cases (possibly 85 to 90 percent) are caused by a dominant mutation in a gene coding for type 1 collagen (Types I, II, III, and IV in the following list). Types V and VI do not have a type 1 collagen mutation, but the genes causing them have not yet been identified. Types VII and VIII are newly discovered forms that are inherited in a recessive manner, and the genes causing these two types have been identified. The general features of each of the known types of OI, which vary in characteristics and severity, are as follows:

• Type I OI• most common and mildest type of OI • bones predisposed to fracture (most fractures occur before puberty) • normal or near-normal stature • loose joints and muscle weakness • blue, purple, or gray tint to sclera (whites of the eyes) • triangular face • tendency toward spinal curvature • absent or minimal bone deformity • possible brittle teeth • possible hearing loss, often beginning in early twenties or thirties • normal collagen structure, but less than normal amount

• Type II OI• most severe form of OI • frequently causes death at birth or shortly after,

because of respiratory problems • numerous fractures and severe bone deformity • small stature with underdeveloped lungs • blue, purple, or gray tinted sclera • improperly formed collagen

• Treatment• There is not yet a cure for OI. Treatment is directed toward

preventing or controlling the symptoms, maximizing independent mobility, and developing optimal bone mass and muscle strength. Care of fractures, extensive surgical and dental procedures, and physical therapy are often recommended for people with OI. Use of wheelchairs, braces, and other mobility aids is common, particularly (although not exclusively) among people with more severe types of OI.

• Doctors frequently consider a surgical procedure called “rodding” for people with OI. This treatment involves inserting metal rods through the length of the long bones to strengthen them. The treatment also prevents or corrects deformities. For more information, see the Osteogenesis Imperfecta Foundation’s fact sheet, Rodding Surgery.

• Scientists are exploring several medications and other treatments for their potential use to treat OI. These include growth hormone treatment, intravenous and oral drugs called bisphosphonates, an injected drug called teriparatide (for adults only), and gene therapies. It is not clear whether people with recessive OI and those with dominant OI will respond to these treatments in the same manner. The OI Foundation can provide current information on research studies and experimental treatments to help individuals with OI decide whether to participate in clinical trials.

• People with OI are encouraged to exercise as much as possible to promote muscle and bone strength, which can help prevent fractures. Swimming and water therapy are common exercise choices for people with OI, as water allows independent movement with little risk of fracture. For those who are able, walking (with or without mobility aids) is excellent exercise. People with OI should consult their doctor or physical therapist to discuss appropriate and safe exercise.

• Children and adults with OI also will benefit from maintaining a healthy weight, eating a nutritious diet, and avoiding activities such as smoking, excessive alcohol and caffeine consumption, and taking steroid medications—all of which may deplete bone and exacerbate bone fragility. For more information on nutrition, see the Osteogenesis Imperfecta Foundation’s fact sheet, Nutrition.

• Prognosis• The prognosis for a person with OI varies greatly

depending on the number and severity of symptoms. Respiratory failure is the most frequent cause of death for people with OI, followed by accidental trauma. Despite numerous fractures, restricted activity, and small stature, most adults and children with OI lead productive and successful lives. They attend school, develop friendships and other relationships, have careers, raise families, participate in sports and other recreational activities, and are active members of their communities.