Clubfoot is the common name used to describe the condition talipes equinovarus, in which there is a deformity of the foot or feet that affects children at birth.  Clubfoot may be classified as congenital (i.e. existing at birth) or teratologic (in which it is associated with a neuromuscular disorder).  The vast majority of cases of clubfoot are congenital, so this form of the condition will be the focus of this summary.  Congenital talipes equinovarus is also known as ‘CTEV,’ an acronym commonly used by orthopaedic surgeons, and this label may be used interchangeably with ?clubfoot’ or ‘idiopathic clubfoot,’ which means that there is no identified cause for the condition.

Babies born with clubfoot have a number of abnormalities of the foot and lower leg, each with varying degrees of severity.  The back portion of the foot is tilted inward, a condition known as hindfoot varus.  The heel is pulled upward, as if to allow walking on the toes, a condition known as hindfoot equinus.  The toes are often pointed inwards, also known as forefoot adduction, giving the foot the appearance of a kidney bean.  The foot will often have a high arch, a configuration termed midfoot cavus.  The foot is generally less flexible and more rigid than normal and there may be thinning, or atrophy, of the muscles of the foot and the calf.  The bones of the foot and the lower leg may not demonstrate normal or complete growth, also known as hypoplasia.  Different patients will show different sets of abnormalities and some may be more prominent than others.  Treatment is therefore somewhat variable and should be catered to each individual’s presentation.  Most patients can be effectively treated with manipulation, casting, and splinting while others may require surgery.



  • Clubfoot has been a recognized condition since the time of the ancient Egyptians, and the condition was independently described by Hippocrates and the Aztecs.
  • Despite knowing about the condition for many centuries, it is still considered idiopathic, which means that its cause is unknown. (The likely factors that contribute to its development are discussed below in the section, ?What causes clubfoot?’)
  • The incidence (i.e., how often it occurs) of the condition varies with race, sex, and familial incidence:
  • Boys are twice as likely to get the disease as girls
  • The incidence among Caucasians is around 1 per 1,000 live births
  • The incidence among children in Japan is 0.5 per 1,000 live births
  • The incidence among natives of the South Pacific is nearly 7 per 1,000 live births
  • The incidence for children who have a sibling with clubfoot is approximately 3%
  • The incidence for children who have 1 parent that had clubfoot is 3-4%; if both parents had it, the incidence is 15%
  • Children born with clubfoot have a higher-than-normal incidence (around 14%) of other genetic conditions, including Edward’s Syndrome , Larsen’s syndrome, spina bifida, neural tube defects, and congenital heart defects
  • Approximately 40% of children with clubfoot will have the abnormality in both feet
  • Clubfoot is generally completely painless.

The normal foot

The foot has a complex musculoskeletal structure, consisting of 26 bones with different shapes and connections.  The bones are attached to each other and to the lower leg bones by an integrated meshwork of thick, fibrous structures known as ligaments.  The areas in which two bones make contact with each other are lined with smooth, slippery cartilage, allowing them to slide past each other with minimal friction.  These areas are the joints and there are many joints in the foot, which collectively allow for movement in the foot and ankle.  Most of the movement of the foot occurs in the base of the foot, in a joint formed between 3 bones, known as the talus, calcaneus, and navicular.  This joint, also known as the talocalcaneonavicular complex, resembles a ball-and-socket joint.  Because of the extensive connections of all the bones of the foot by the ligaments, motion in the foot and ankle joints occurs at all joints simultaneously, with motion in one joint leading to motion in others.  At the same time, if motion is limited in one or more joints, motion is limited in many other joints.


As mentioned above, the cause of clubfoot remains unclear.  There is strong evidence that a genetic component is involved in the development of clubfoot.  For example, approximately 25% of affected children have a relative who was born with the condition, and if an identical twin has the condition, the other twin (who has the same set of genes) has a much higher incidence of the condition than normal.  However, no single gene has been identified as being responsible for the condition.   Rather, it is believed that the cause is multifactorial , in which a number of different genes and non-genetic factors are involved.   There is ongoing research at various medical centers in the U.S., dedicated to identifying these factors and improving the treatment of clubfoot.

The central problem in clubfoot lies in the abnormal shape of the bones of the feet, the misaligned joints and the tightening of the ligaments around these irregular alignments during fetal life.  These changes cause the foot and ankle to become deformed and remain in an abnormal position through the time of birth.


The diagnosis of clubfoot is made by physical examination soon after birth.   However because prenatal ultrasound has become more common and more technologically advanced in the last fifteen years or so, the diagnosis of clubfoot is occasionally made before birth.

In severe cases of clubfoot, other tests may be performed to solidify the diagnosis of clubfoot or to investigate the possibility of other abnormalities.   These include x-ray, ultrasound, CT scan, MRI, and genetic testing. However, use of diagnostic tests other than a few x-rays is rare.


Initially, all children are treated non-operatively (i.e., with treatments other than surgery), no matter how severe their clubfoot may be.  This non-operative treatment involves weekly visits to the office for manipulation to improve the alignment of the foot, followed by application of a long leg cast to maintain the new alignment.  Generally 5 to 8 casts are required to correct the clubfoot.  All of the deformities are corrected with the casting except for the hindfoot equinus.  This usually requires a percutaneous Achilles tenotomy (cutting of the Achilles tendon).  Following this procedure the child will be placed back into a cast for 3 more weeks.  The cast is then removed and boots connected by a bar are used to maintain the correction.  This is a very important part of the treatment.  The boots and bars are worn full-time for 3-4 months.  Following this, they are worn for nights and naps until the child is 3-4 years of age.

In rare instances, non-operative measures fail to correct the deformity effectively, and surgery becomes the recommended treatment.  If surgery is going to be performed, the optimal time in a child’s life is between 6 and 12 months of age.  Studies have suggested that surgery during this time frame will minimize scarring, which can occur with younger children, while maximizing the opportunity for growth and remodeling of the bones and muscles of the foot and ankle, which occurs rapidly in the first year of life.

The actual operation that is performed involves performing soft tissue release in multiple regions, which means loosening several of the abnormally tightened ligaments or tendons, such as the Achilles tendon, in order to realign the foot properly. Placement of a cast on the lower leg and foot is also a basic part of treatment, and this may occur either in the operating room immediately following the surgery or 1 week following the surgery.  To maximize the healing of the foot and ankle following the operation, this cast must be worn for a period of 4-6 weeks.  Many orthopaedic surgeons also prescribe the use of a splint after the cast is taken off, which children may be asked to wear for up to 2 years.


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JL Taman Bendungan Asahan 5 Jakarta Indonesia

phone : 62(021) 70081995 – 5703646

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Copyright © 2009, Clinical Pediatric Food Allergy Information Education Network. All rights reserved.


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