Clubfoot is a congenital deformity in which an infant’s foot is twisted out of its normal shape or position. The medical term for the most common type of clubfoot is talipes equinovarus, which can be broken down from Latin to describe the foot’s appearance:

• Talipes: A term for the foot and ankle.
• Equinus: Meaning “horse-like,” this refers to the foot being pointed downward, with the heel drawn up.
• Varus: Refers to the heel being turned inward.

The core problem in a true clubfoot is not that the bones are misshapen, but that the tendons and ligaments on the inside and the back of the foot are abnormally short and tight. These tight connective tissues act like powerful tethers, pulling the foot into its abnormal position.

A helpful analogy is to think of the bones of the foot as the flexible wooden frame of a tent.

• The tendons and ligaments are the ropes and stakes that hold this frame in place and give it its shape.
• In a normal foot, the “ropes” on all sides have equal tension, holding the tent in a perfect, stable shape.
• In a clubfoot, it is as if the ropes on the inside and the back of the tent were manufactured too short and have been pulled incredibly tight.
• These tight ropes pull the entire tent frame inward and downward into a twisted position.

The goal of treatment is not to break or reshape the tent poles (the bones), but to gently and gradually stretch the tight ropes until the frame can be moved back into its correct, functional alignment.

In my experience, parents are often alarmed at birth when they notice their baby’s foot turned inward or downward, but with early treatment, the long-term outlook is usually very positive.

The exact cause of isolated clubfoot is unknown. It is not caused by the baby’s position in the womb. This distinguishes a true, rigid clubfoot from a milder “positional clubfoot,” where the foot was simply held in an awkward position in utero and is flexible and easily corrected.

It is believed that clubfoot is a multifactorial condition, meaning it likely results from a complex combination of genetic and environmental factors that interact during fetal development to affect the growth of the muscles, tendons, and ligaments of the foot.

Clinically, most cases are idiopathic, meaning no clear cause is identified. But I often see it linked to limited space in the womb, genetic predisposition, or neuromuscular disorders.

Clubfoot is a congenital condition, meaning it is present at birth, and the developmental error occurs early in pregnancy. It is not contagious and is not caused by anything the parents did or did not do during the pregnancy.

The primary risk factors for developing clubfoot include:

• Genetics: A family history is the strongest risk factor. If a parent or a previous child has a clubfoot, the risk of a subsequent child having the condition is significantly higher.
• Gender: Clubfoot is about twice as common in boys as it is in girls.
• Associated Conditions: While most cases of clubfoot are isolated (idiopathic), it can sometimes be associated with other neuromuscular or genetic conditions, such as spina bifida.

In my experience, it usually develops during fetal development, possibly due to genetic and mechanical factors affecting the bones and tendons of the foot.

Clubfoot signs are purely physical and are usually obvious at birth. The condition can affect one foot (unilateral) or both feet (bilateral).

The hallmark signs of a clubfoot’s position can be remembered by the acronym CAVE:

• Cavus: The arch of the foot is abnormally high.
• Adductus: The front of the foot (the forefoot) is turned inward, toward the other foot.
• Varus: The heel is turned inward.
• Equinus: The entire foot is pointed downward, with the heel raised and the toes pointing toward the ground.

Other physical signs include:

• The affected foot, calf, and leg may be slightly smaller and shorter than the unaffected side.
• The foot is very rigid and cannot be manually manipulated into a normal position.

It is very important for parents to know that the clubfoot deformity itself is not painful for a newborn baby.

Clinically, I assess for the rigidity of the deformity, calf muscle underdevelopment, and any associated hip or spinal anomalies, especially in non-idiopathic cases.

The diagnosis of clubfoot is typically very straightforward.

• Prenatal Diagnosis: In many cases, clubfoot is first detected during a routine second-trimester prenatal ultrasound. While an ultrasound cannot determine the severity or rigidity of the foot, it allows parents to be aware of the diagnosis ahead of time. This provides a valuable opportunity to meet with a pediatric orthopedic specialist, learn about the condition, and prepare a treatment plan that can begin shortly after birth.
• Postnatal Diagnosis: If not diagnosed prenatally, the condition is diagnosed immediately at birth based on a visual physical examination by a pediatrician or orthopedic surgeon. The characteristic twisted appearance of the foot is unmistakable.

No X-rays or other imaging tests are needed to diagnose clubfoot in an infant. The diagnosis is clinical, based entirely on the physical appearance of the foot.

In my experience, imaging isn’t always necessary for diagnosis, but I use it to evaluate severity or plan treatment in complex or atypical cases.

The goal of clubfoot treatment is to correct the deformity in order to provide a patient with a functional, flexible, and pain-free foot that allows them to wear normal shoes and lead a normal, active life.

The modern gold standard for treating congenital clubfoot is a non-surgical technique known as the Ponseti method. This method has revolutionized clubfoot care and has nearly eliminated the need for extensive surgery in infants.

The Ponseti method is a staged process involving gentle manipulation, casting, and bracing. Phase 1: Serial Manipulation and Casting (The Correction Phase)

• Timing: Treatment should begin as early as possible, ideally within the first one to two weeks of life, when the baby’s tendons and ligaments are at their most elastic.
• Process: The process involves a series of weekly visits to a specially trained pediatric orthopedic specialist.
  • At each visit, the doctor performs a gentle manipulation of the foot, stretching the tight ligaments and tendons in a specific, sequential order.
  • After each manipulation, a long-leg, plaster cast is applied, extending from the toes to the upper thigh with the knee bent. This cast holds the foot in its newly corrected position for the next week.
  • This process is repeated every week for approximately 5 to 8 weeks. Each week, the old cast is removed, the foot is stretched a little further into a more corrected position, and a new cast is applied to hold the gains.

Phase 2: Achilles Tenotomy

• After the casting phase has corrected the main parts of the deformity, the equinus (the downward-pointing of the foot) usually remains due to a very tight Achilles tendon (heel cord).
• In over 90% of cases, a minor procedure called an Achilles tenotomy is needed.
• This is a simple procedure, often performed in the clinic under local anesthesia. The doctor uses a tiny blade to make a small, precise clip in the Achilles tendon. This releases the tension and allows the heel to drop into a normal position. The tendon then heals and regrows to its new, proper length over the next three weeks inside a final cast.

Phase 3: Bracing (The Maintenance Phase)

This is the most critical part of the Ponseti method for preventing a relapse. The foot has a strong natural tendency to want to twist back into its old clubfoot position. The bracing protocol is essential to hold the correction until the child’s foot has grown and the muscle balance has been established.

• The Brace: The brace consists of two shoes or sandals attached to a metal bar at a specific width and angle of external rotation. This is often called a “boots and bar” or Denis Browne bar.
• The Schedule:
  • The child must wear the brace for 23 hours a day for the first three months after the last cast is removed.
  • After that, the brace is worn only at nighttime and during naps until the child is approximately 4 to 5 years old.
• Adherence: Strict, consistent adherence to the bracing schedule is absolutely essential for a successful long-term outcome. Failure to follow the bracing protocol is the number one cause of clubfoot relapse.

Surgery

Before the widespread adoption of the Ponseti method, extensive “comprehensive clubfoot release” surgery was the standard treatment. Today, this major surgery is considered a last resort. It is reserved for the small percentage of children whose feet do not fully correct with the Ponseti method, for those who experience a relapse due to non-adherence with bracing, or for older children with neglected or previously untreated clubfoot.

Clinically, I emphasize early treatment within the first weeks of life to achieve the best outcomes. Parents play a vital role in brace compliance post-correction.

A diagnosis of clubfoot can be an emotional and daunting experience for new parents. It is essential to be armed with the knowledge that this common birth defect is highly correctable. The development of the Ponseti method has been a true medical miracle, transforming clubfoot from a lifelong disability requiring extensive surgery into a manageable condition that can be corrected with a gentle series of casts and a dedicated bracing regimen. While the process requires a significant commitment and partnership between parents and their orthopedic team, the result is a priceless gift. Clinically, I reassure families that although clubfoot looks severe at birth, it is one of the most successfully treated congenital musculoskeletal conditions with modern methods.

Ponseti International Association. (n.d.). The Ponseti Method. Retrieved from https://www.ponseti.info/

American Academy of Orthopaedic Surgeons (AAOS). (n.d.). Clubfoot. Retrieved from https://orthoinfo.aaos.org/en/diseases–conditions/clubfoot/

The Mayo Clinic. (2022). Clubfoot. Retrieved from https://www.mayoclinic.org/diseases-conditions/clubfoot/symptoms-causes/syc-20353386