National Organization for Rare Disorders, Inc.
It is possible that the main title of the report Clubfoot is not the name you expected. Please check the synonyms listing to find the alternate name(s) and disorder subdivision(s) covered by this report.
- Calcaneal Valgus
- Metatarsus Varus
- Talipes Calcaneus
- Talipes Equinovarus
- Talipes Equinus
- Talipes Valgus
- Talipes Varus
- Valgus Calcaneus
Clubfoot is a general term used to describe a group of deformities of the ankles and/or feet that are usually present at birth (congenital). The defect may be mild or severe and may affect one or both of the ankles and/or feet. Different forms of clubfoot may include talipes equinovarus in which the foot is turned inward and downward; calcaneal valgus in which the foot is angled at the heel with the toes pointing upward and outward; and metatarsus varus in which the front of the foot is turned inward. If not corrected, affected individuals may develop an unusual manner of walking (gait) in which weight is placed on the side of the foot (lateral) rather than on the sole. Clubfoot may be caused by a combination of hereditary and other factors (e.g., environment) and may occur as an isolated condition or due to a number of different underlying disorders.
There are several types of clubfoot. They are as follows:
The foot is turned inward and downward . If both feet are affected the toes point toward each other instead of straight ahead. The heel cord often is very tight, making it impossible to bring the foot up to a normal position without a specialist's help.
Calcaneal Valgus or Valgus Calcaneus
This type of clubfoot is more common. The foot is sharply angled at the heel, with the foot pointing up and outward.
The front part of the foot is turned inward.
The front part of the foot is turned inward and inverted. Although present at birth, this form of abnormality may not be diagnosed until the infant is a month to a few months old. With treatment the foot can look better and become more functional.
In general, clubfoot is not painful and doesn't bother the baby until he or she begins to stand and walk. Since the ankle is twisted in place, the foot can't move up and down as it normally would in walking. The child must walk as if he were on a peg leg.
If both feet are affected, the child walks on the balls of his feet. If the feet are badly twisted, the child will walk on the sides or even the top part of the feet instead of the soles. The part that comes in contact with the ground may become ulcerated, hard and lumpy, since it is not protected by the thick skin of the sole of the foot. The entire leg is sometimes unable to grow as it should.
The exact cause of clubfoot is not fully understood. In the past, it was thought to be caused by a twisting of the fetus' feet in the mother's womb. However, this has been found to be true only when the problem resolves spontaneously after birth. Many scientists think the defect starts as early as the eighth week of pregnancy before the fetus is large enough to stay in one position very long.
Clubfoot probably is caused by a combination of hereditary and other factors that may affect prenatal growth, such as infection, drugs, disease or other factors in the environment.
During pregnancy, the tendons on the inside of the lower leg become shortened (for unknown reasons) and this shortening when combined with unusually shaped bones causes the foot to turn inward. The Achilles tendon becomes tense or tightened causing the foot to point downward.
Although most children with clubfoot have no other birth defects, occasionally there are other abnormalities as well. Children with an open spine (spina bifida) sometimes have a form of clubfoot. This is caused by damaged spinal nerves that affect the leg muscles. In other cases, feet that are normal at birth may become twisted as a result of muscle or nerve disease.
Clubfoot is usually present at birth. Approximately 9,000 babies (about one in 400 live births) are born annually in the United States with this congenital defect. Boys are affected twice as often as girls.
Clubfoot is usually apparent on physical examination at birth.
Treatment of clubfoot is started soon after birth.
There are differences of opinion between "conservative" treatment that consists of the use of plaster casts or their stand-ins, and "radical" treatment that usually makes use of surgery. Within conservative treatment there are debates about the alternative methods of casting.
Serial casting involves the manipulation of the foot to a position as far forward as far as it can go, followed by plaster casting to hold it in that position. At first, the cast is changed to bring the foot closer to normal through frequent adjustments. After the foot is straightened, it is tilted further upward to stretch the tightened heel cord. It is kept in this over-corrected position for a few weeks. The treatment usually requires three to six months, followed by checkups for many years by an orthopedist.
The Ponseti method involves manipulation, casting and limited surgery.
An evaluation of the two methods for treatment of idiopathic clubfoot showed the Ponseti method to be more effective and economic.
In certain cases, some doctors use adhesive bandaging over a special type of splint instead of hard casts. After the bandages are off (or in some mild forms of clubfoot), the baby sleeps in shoes attached to a metal bar that holds the feet in a corrected position.
Sometimes the heel cord is too tight to be stretched by a cast or bandaging, and the patient must undergo surgery to lengthen it.
Immediate treatment for clubfoot using casts or strapping (not surgery), works in more than half of the cases.
With expert early treatment, most patients grow up to wear regular shoes, can take part in sports, and lead full, active lives.
Investigators from the Intermountain Unit of Shriners Hospitals for Children, the University of Utah Department of Pediatrics, and the Eccles Institute of Human Genetics are collaborating on a project to map and characterize genes causing multiple congenital contracture disorders and limb deficiency/duplication syndromes. The disorders being studied are: autosomal dominant clubfoot, distal arthrogryposis type I, Gordon Syndrome, Freeman-Sheldon Syndome, Trismus Pseudocamptodactyly, autosomal dominant Multiple Pterygium Syndrome, autosomal ulnar hypoplasia ectrodactyly disorders, ulnar mammary syndrome, Holt-Oram Syndrome, and fibular hypoplasia. For more information, please contact:
Michael Bamshad, M.D.
Eccles Institute of Human Genetics
Building 533 Room 2100
University of Utah Medical Center
Salt Lake City, UT 84112
Tel: (801) 585-3384 office
Tel: (801) 585-3385 lab
Fax: (801) 581-7796
Information on current clinical trials is posted on the Internet at www.clinicaltrials.gov. All studies receiving U.S. government funding, and some supported by private industry, are posted on this government web site.
For information about clinical trials being conducted at the NIH Clinical Center in Bethesda, MD, contact the NIH Patient Recruitment Office:
Tollfree: (800) 411-1222
TTY: (866) 411-1010
For information about clinical trials sponsored by private sources, contact:
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