SOMETHING EXTRA...
Clubfeet share a set of common CHARACTERISTICS, typical for all types. However, there are some feet that have additional features in their structure.
Atypical and complex clubfeet are specific deformities with their own additional characteristics, which develop at certain times and due to specific factors. Unfortunately, the terms atypical and complex clubfoot are often used interchangeably, which leads to much confusion in distinguishing between these two types. It is, however, very important to recognize them correctly.
Understanding the development and structure of atypical and complex clubfeet is crucial, as these feet require modifications in treatment — starting from manipulation and casting, and later in the adjusted settings of the abduction brace. Such feet also carry different prognoses regarding relapse and potential future treatments.
Early identification of atypical and/or complex clubfoot, along with modification of the standard treatment protocol as described by Ponseti, is critical to achieving effective correction.
ATYPICAL CLUBFOOT
Atypical clubfoot is a variant of non-standard deformity that can be recognized immediately after birth, even before any treatment begins. This is because it has additional structural (and visible) features. Failure to correctly identify it leads to the use of inappropriate treatment, which in turn aggravates its existing characteristics and may result in the development of a complex clubfoot.
Atypical clubfoot usually appears as a variant with neurological or syndromic etiology. Patients with this deformity often show weak or absent active dorsiflexion of the toes during stimulation, limited dorsiflexion of the foot, and significantly reduced eversion. These signs are associated with neurological and/or motor deficits.
On its own, atypical clubfoot is relatively rare — it affects less than 5% of children, which makes it a small proportion compared to other types of clubfoot.
CHARACTERISTICS
An atypical clubfoot does not show marked adduction. Instead, it is usually moderate, which may give the misleading impression that treatment will be easier. However, during the course of treatment, many difficulties arise in achieving proper correction.
A shortened plantar fascia positions all the metatarsal bones in plantar flexion, most notably the first one. As a result, a deep transverse crease forms on the sole of the foot, running from the inner to the outer side. It gives the appearance as if the foot were “broken in half” at the midfoot.
The combination of the metatarsals plantar flexion and the strong pull of a short and thick Achilles tendon causes a deep crease to form above the heel. Despite this, the ankle joint itself is not stiff. The outline and shape of the heel remain unchanged. When viewed from the sole, the heel most often takes the shape of a “V” or a very tight “U.” From behind, it gives the impression of being very soft. The thick fatty tissue inside the heel makes it difficult to palpate the calcaneus, which creates the impression that the heel is soft and hollow.
Plantar flexion of the first metatarsal bone, caused by a shortened plantar fascia and weakness of the toe extensors, makes the first ray appear shortened, while the big toe points upward. The other toes may be curled, may take on a hammer-like shape, and show a very weak response to stimulation, such as gentle irritation.
COMPLEX CLUBFOOT
Complex clubfoot is a variant of non-standard deformity that occurs relatively more often compared to atypical clubfoot. Importantly, a complex foot can develop from any type of clubfoot, regardless of etiology or the original range of motion.
This is a typical iatrogenic deformity, meaning that complex clubfoot is the result of improper treatment — such as incorrect casting technique, frequent cast slippage, or casting on a swollen leg. It is therefore dependent on external factors, where the physician’s understanding of the pathoanatomy of clubfoot, knowledge of the Ponseti method, and technical skill all play a crucial role. Because this deformity arises as a consequence of inadequate treatment, it cannot be diagnosed prenatally or on ultrasound.
Due to poor-quality treatment, the foot develops additional structural deformities, which give it extra visible features. Physicians sometimes refer to this type of foot as “resistant”, because even after 4–5 casts, the foot not only fails to improve but actually worsens and becomes more difficult to correct.
Children who develop this type of foot often struggle with serious skin problems under the cast: redness, wounds, abrasions, significant swelling, and bruising. These complications further worsen the situation and increase the complexity of the deformity. Poorly applied casts may slip, the foot may slide out or get wedged, the skin becomes stiff as in lymphedema, and the slipping cast can create new deformities or reinforce existing ones.
The risk of soft tissue surgery, which may eventually become necessary, ranges from 3% to 5%.
CHARACTERISTICS
Due to casts frequently slipping off, the foot becomes wedged inside them. This causes the calcaneus to be artificially lifted, resulting in a severe equinus position of 50° to 70°. In some cases, the proximal part of the calcaneus comes into contact with the distal fibula and becomes locked there. As a result, the Achilles tendon becomes extremely tight, thickened, and fibrotic up to the mid-calf. Similarly, the gastrocnemius muscle is reduced in size and volume, concentrated in the upper part of the calf.
The Achilles tendon pulls the calcaneus strongly upward, with the external sign being a deep crease above the heel. The outline and shape of the heel are also altered: it often appears misshapen, flattened, compressed, or tilted. The thick fatty tissue inside the heel makes the calcaneus difficult to palpate, giving the impression that the heel is soft and hollow.
Because all the metatarsal bones are strongly plantarflexed due to an excessively shortened plantar fascia, the foot develops a high arch, and a deep transverse crease forms on the sole. It gives the appearance as if the foot were “broken in half.” At the same time, the foot becomes noticeably shorter (for example, in unilateral cases, the affected foot may be 1.5–2 cm shorter than the healthy one).
A large amount of fatty tissue accumulates on the dorsum of the foot, giving the impression that the foot is permanently swollen. This makes it difficult to properly grasp the foot before performing manipulation and applying a cast, as the foot is short and the fatty tissue is dense.
Plantar positioning of the metatarsal bones and an excessively shortened plantar fascia, according to the Hicks mechanism, cause the big toe to be excessively extended upward (hyperextension). As a result, it appears to be “pushed” deep into the foot, and the first ray becomes shortened.
TREATMENT
Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
"GROTUESQUELY DEFORMED FOOT"
Treatment with the Ponseti method is highly effective, allowing feet to regain full functionality and a normal appearance. This high success rate and relative ease of treatment applies to the vast majority of clubfeet. However, some cases are resistant to standard manipulation and casting — namely, atypical and complex clubfeet.
As early as 1994, Dr. Vincent J. Turco noted that these feet “respond very differently to operative and non-operative treatment, and early surgery leads to a grotesquely deformed foot.” He was the first to describe them as “atypical clubfoot” and advised against any surgical intervention on such feet.
In 2006, Dr. Ignacio Ponseti and his colleagues reported changes to the standard treatment protocol, introducing a modified Ponseti protocol for these cases.
In this modified protocol, both the manipulation techniques performed before casting and the casting process itself differ from the classical approach. After the necessary tenotomy, plaster casts may need to be changed more frequently than in standard treatment. The use of the abduction brace is also adjusted — including its wear schedule, positioning, and even the type of brace used.
The key element of this treatment protocol is the very precise localization of the talar head and strict adherence to the individual steps carefully described by Dr. Ignacio Ponseti.
The deformity is difficult to treat because, although forefoot adduction can usually be corrected after the first or second manipulation and casting, the metatarsal bones remain rigidly plantarflexed, and the calcaneus remains fixed in an equinus position. Additional attempts to correct hindfoot varus by abducting the foot result in over-abduction of the strongly plantarflexed metatarsals. Because of the rigid and severe equinus of both the calcaneus and the metatarsals, casts slip easily, which worsens the deformity and damages the swollen skin on the dorsum of the foot. To correct hindfoot varus in complex clubfoot, the hindfoot must be abducted while counterpressure is applied not only on the head of the talus but also on the lateral malleolus. The forefoot should not be abducted beyond its normal alignment. Once hindfoot varus is corrected, the plantarflexed forefoot and valgus deformity can be corrected simultaneously by forcefully dorsiflexing the metatarsals with both thumbs while applying a reinforcing plaster cast.
Let us now take a closer look at each step to make the treatment process clearer.
STEP 1 – 30°–40° AND NO MORE: CORRECTING ADDUCTION
In the standard treatment protocol consistent with the principles of the Ponseti method, applying counterpressure to the talus from the lateral side and slowly abducting the foot in supination allows free movement of the calcaneus, thereby achieving correction.
However, in atypical and complex clubfeet, this maneuver cannot be used. It would cause excessive abduction of the forefoot at the Lisfranc joint and even greater plantarflexion of the metatarsals and toes. This is due to the shortened and tight deep plantar muscles. A visible sign of such an incorrect maneuver is a deep crease along the lateral border of the foot.
To ensure the correct position of the talar head during manipulation (and later when applying the plaster cast), the index finger should rest on the posterior aspect of the lateral malleolus, while the thumb of the same hand applies counterpressure to the lateral side of the talar head — not to the prominent anterior tuberosity of the calcaneus. To avoid abduction at the Lisfranc joint, only 30°–40° of abduction is allowed — and no more! Forefoot adduction is usually corrected easily after one or two manipulations and the application of one or two plaster casts in the position described above, changed weekly.
STEP 2 – SIMULTANEOUSLY: CORRECTING METATARSAL FLEXION AND EQUINUS
After achieving 40° of foot abduction, the method of manipulation must be changed, because the metatarsal bones remain in strong plantarflexion and the hindfoot remains in severe equinus. The aim of this adjustment is to simultaneously correct both the plantarflexion of the metatarsals and the severe equinus of the calcaneus.
For this purpose, both index fingers should be placed on either side of the talar head, with the thumbs positioned on the first and fifth metatarsal heads (“four fingers” technique). An assistant holds the leg with the knee flexed. The physician then slowly lifts all the metatarsals toward a neutral position, while allowing the trapped calcaneus to move out from under the talus. Care must be taken not to over-abduct either the metatarsals or the hindfoot.
The manipulation focuses on stretching the tightly contracted plantar fascia and the tendons of the plantar and medial side of the foot.
Improper cast molding
CASTS
A complex clubfoot develops as a result of improper casting — the casts are poorly molded, often slip off, the foot becomes wedged inside, swelling occurs, fatty tissue shifts into certain areas, and bruising appears. Applying another cast on such a foot only creates additional deformities and makes them permanent. The first step is to remove a slipping cast immediately! The second step is… to change the doctor.
Before restarting treatment and recasting, it is essential to allow time for the swelling in the leg and foot to subside. Casting a swollen foot and leg is pointless and only leads to further complications. Sometimes the break from casting may be long. The foot may return to its faulty original position, but this is actually better before resuming treatment than applying plaster casts over swelling.
A full cast is applied, extending from the toes to the groin, exactly as in the standard Ponseti protocol. However, to prevent the cast from slipping off a stocky foot, the leg should be bent at the knee at 110–120° (not 90°) during casting, and the cast applied in this position.
The cast is additionally reinforced: a plaster splint is applied to the calf, heel, and sole, and then fully wrapped with plaster. This helps avoid excess plaster in front of the ankle joint. A small plaster splint is also placed over the front of the knee, then fully wrapped, to prevent excess plaster behind the knee. The cast at the front of the thigh may be gently flattened at the top, while the talar region and foot are carefully molded.
The toes should rest on a stable plaster platform beneath them. Without this support, the already overactive plantar flexors act even more strongly. The platform stretches them evenly and effectively disengages the Hicks windlass mechanism, contributing to correction of the cavus deformity and excessive hallux hyperextension. All toes should remain visible, side by side, in one line — not curled, not overlapping. However, they should not be left exposed, as is standard in the Ponseti method, because in this case it is necessary to secure the big toe to prevent it from being excessively extended.
Typically, 5–8 plaster casts are sufficient to correct the deformity (with exceptions in more difficult cases, e.g., clubfoot in children with arthrogryposis).
Proper cast molding
STEP 3 – PERCUTANEOUS ACHILLES TENDON TENOTOMY
A percutaneous Achilles tendon tenotomy is necessary in almost all cases. It is performed once the physician has achieved slight abduction of the foot (up to about 30°) and correction of excessive plantarflexion of the metatarsals, while equinus persists (the equinus deformity is not fully corrected). An earlier tenotomy may be required if the cast slips off too frequently or if the foot is so deformed that the calcaneus is locked near the fibula in severe plantarflexion, preventing any movement and making it impossible to achieve 30° of foot abduction.
The tendon is cut approximately 1.5 cm above the crease visible above the heel. This distance helps avoid injury to the posterior tuberosity of the calcaneus, which is positioned very high due to the severe equinus deformity. To achieve correction, at least 10° of dorsiflexion is required. If this is obtained during the procedure, the final cast is applied for 3–4 weeks in a maximum of 40° of abduction.
When 10° of dorsiflexion cannot be achieved during the procedure due to severe equinus of the calcaneus, the casts are then changed weekly (from one to four times) until both abduction of the foot (up to 40°) and dorsiflexion (at least 5°, preferably 10°) can be obtained.
STEP 4 – FOOT ABDUCTION BRACE
Parent education is key when it comes to the effective use of the abduction brace, which is applied immediately after the cast is removed following percutaneous Achilles tendon tenotomy.
The shoes must be carefully made and properly fitted to prevent the feet from slipping out, and the foot abduction brace must be correctly adjusted. The Mitchell brace provides this level of security. The standard Denis Browne bar with lace-up shoes is not sufficient for this type of foot: the foot often slips out, losing correction. It is also difficult to control heel position inside the shoe — which is critical.
The initial brace setting should be 20°–40° of abduction (studies show varying values, though 40° is most common), depending on whether the foot is atypical or complex. Later, as the foot begins to take on a near-normal shape, abduction may be increased to 50°, and should then be gradually increased every few weeks until reaching 60°.
The brace is used until the age of 5 years to prevent relapse.
TECHNIQUE-NOT THE FOOT
Very often, a typical, standard clubfoot is turned into a complex clubfoot because of poor casting. In such cases, many parents are told: “This foot is difficult, uncorrectable, stiff” — and that surgery will surely be needed because the doctor cannot achieve correction.
Many physicians are not even aware that they are creating such feet. They frequently dismiss this type of deformity, telling parents: “You took poor care of your child, you carried them wrong, and that’s why the cast slipped or fell off.”
THIS IS NOT TRUE!
Transforming a standard clubfoot into a complex clubfoot is never the fault of the foot itself — it is ALWAYS the result of poor casting technique.
THE RISK OF RELAPSE
In atypical and complex clubfeet, the relapse rate is as high as 68%, and unlike in standard clubfoot, it does not decrease with prolonged use of the abduction brace. This is a significant figure, and families must be prepared for different scenarios. Unfortunately, to date, no studies have distinguished relapse risk separately for atypical versus complex clubfeet.
Nevertheless, despite this high risk of relapse, treatment with the Ponseti method in children aged 4–10 years yields very good results in the early stages, significantly reducing the need for invasive surgery. In some cases of relapse, repeating proper casting or performing a simple procedure such as anterior tibial tendon transfer (ATTT) or a minimally invasive percutaneous triple hemisection (Hoke’s technique) can be effective alternatives to invasive surgeries, such as extensive releases — including posteromedial release. Dr. Vincent J. Turco himself stated that such releases create an additional problem: overcorrection leading to a rigid flat-valgus foot. The earlier such surgeries are performed, the more severe the deformity becomes, resulting in lifelong complications that may not be immediately apparent but develop over time.
In general, there is no need for extensive surgical interventions, since using the modified Ponseti method provides excellent outcomes, even in cases of relapse. When relapse does occur, the standard procedure is simply to return to casting, as described in the article on RELAPSES.
WORDS OF HOPE
Although atypical and, even more so, complex clubfoot are specific examples of deformity, the modified Ponseti method is a safe and effective treatment with excellent long-term results, drastically reducing the need for any surgery — including invasive procedures such as posteromedial release (PMR).
The shape, length, and dorsiflexion of the foot improve within a few months after correction. In addition, the motion of the subtalar joint also normalizes, and over time the foot develops properly, allowing your child to be fully functional.
- Ponseti I.V.: „Congenital Clubfoot. Fundamentals of treatment.” (2nd edition)
- Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Turco V.J.: „Recognition and Management of the Atypical Idiopathic Clubfoot”, Springer-Verlag New York, Inc. 1994
- Gupta A. et al.: „Atypical clubfoot: Early Identification and treatment by modification of standard Ponseti technique.”
- Dobbs M.B., Williams M.: “Congenital Foot Deformities.” | “Pediatric Lower Limb Deformities. Principles and Techniques of Management.” (2nd etition)
- Masquijo J., Arana E.: “Complex clubfoot: my 5 tips for appropriate evaluation nd treatment with the Ponseti method.”
- Chu A. et al.: “Management of complex clubfoot.”
- Rangasamy K. et al.: „Correction results of atypical clubfeet managed with modified Ponseti technique: A meta-analysis of 354 feet.”
- Allende V. et al.: „Complex clubfoot treatment with Ponseti method: a Latin American multicentric study.”
- Yadav A. et al.: „Management of complex idiopathic clubfoot using modified Ponseti method.”
- Rodrigues N. et al.: „Management of Complex Clubfoot: Challenges and Solutions”
- Agarwal A. et al.: „Results of Modified Ponseti Technique in Difficult Clubfoot and a review of literature.”
- Matar H.E. et al.: „Treatment of complex idiopathic clubfoot using the modified Ponseti method: up to 11 years follow-up.”
- Bozkurt C. et al.: „Using the modified Ponseti method to treat complex clubfoot: Early results.”
- Radler C., Herzenberg J.E. et al.: „Ponseti versus traditional methods of casting for idiopathic clubfoot.”
- Ponseti I.V., Morcuende J.A. et al.: „Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method.”
- Bolgla L.A., Malone T.R.: „Plantar Fasciitis and the Windlass Mechanism: A Biomechanical Link to Clinical Practice.”
- Loose O. et al.: “Complex, atypical clubfoot: follow-up after up to 16 years reveals a high risk of relapse but good functional and radiological outcomes”
- Radler C.: “Standard AFO for clubfoot and atypical clubfoot a unified approach.”
- Morcuende J.A.: “Complex Clubfeet: Recognition & Management.”
- Morcuende J.A.: “Pediatric Orthopedics Active learning Session – Management of Relapsed Clubfeet : Dr Jose Morcuende”
- Ponseti International Association (Ponseti I.V.): “Complex Clubfoot at Birith”
In the order of appearance on the page:
-
- 1-3: Own
- Windlass Mechanism
- Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Redressions: Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Redressions: Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- 8-12: Own
SOMETHING EXTRA…
Clubfeet share a set of common CHARACTERISTICS, typical for all types. However, there are some feet that have additional features in their structure.
Atypical and complex clubfeet are specific deformities with their own additional characteristics, which develop at certain times and due to specific factors. Unfortunately, the terms atypical and complex clubfoot are often used interchangeably, which leads to much confusion in distinguishing between these two types. It is, however, very important to recognize them correctly.
Understanding the development and structure of atypical and complex clubfeet is crucial, as these feet require modifications in treatment — starting from manipulation and casting, and later in the adjusted settings of the abduction brace. Such feet also carry different prognoses regarding relapse and potential future treatments.
Early identification of atypical and/or complex clubfoot, along with modification of the standard treatment protocol as described by Ponseti, is critical to achieving effective correction.
ATYPICAL CLUBFOOT
Atypical clubfoot is a variant of non-standard deformity that can be recognized immediately after birth, even before any treatment begins. This is because it has additional structural (and visible) features. Failure to correctly identify it leads to the use of inappropriate treatment, which in turn aggravates its existing characteristics and may result in the development of a complex clubfoot.
Atypical clubfoot usually appears as a variant with neurological or syndromic etiology. Patients with this deformity often show weak or absent active dorsiflexion of the toes during stimulation, limited dorsiflexion of the foot, and significantly reduced eversion. These signs are associated with neurological and/or motor deficits.
On its own, atypical clubfoot is relatively rare — it affects less than 5% of children, which makes it a small proportion compared to other types of clubfoot.
CHARACTERISTICS
An atypical clubfoot does not show marked adduction. Instead, it is usually moderate, which may give the misleading impression that treatment will be easier. However, during the course of treatment, many difficulties arise in achieving proper correction.
A shortened plantar fascia positions all the metatarsal bones in plantar flexion, most notably the first one. As a result, a deep transverse crease forms on the sole of the foot, running from the inner to the outer side. It gives the appearance as if the foot were “broken in half” at the midfoot.
The combination of the metatarsals plantar flexion and the strong pull of a short and thick Achilles tendon causes a deep crease to form above the heel. Despite this, the ankle joint itself is not stiff. The outline and shape of the heel remain unchanged. When viewed from the sole, the heel most often takes the shape of a “V” or a very tight “U.” From behind, it gives the impression of being very soft. The thick fatty tissue inside the heel makes it difficult to palpate the calcaneus, which creates the impression that the heel is soft and hollow.
Plantar flexion of the first metatarsal bone, caused by a shortened plantar fascia and weakness of the toe extensors, makes the first ray appear shortened, while the big toe points upward. The other toes may be curled, may take on a hammer-like shape, and show a very weak response to stimulation, such as gentle irritation.
``ATYPICAL``
COMPLEX CLUBFOOT
Complex clubfoot is a variant of non-standard deformity that occurs relatively more often compared to atypical clubfoot. Importantly, a complex foot can develop from any type of clubfoot, regardless of etiology or the original range of motion.
This is a typical iatrogenic deformity, meaning that complex clubfoot is the result of improper treatment — such as incorrect casting technique, frequent cast slippage, or casting on a swollen leg. It is therefore dependent on external factors, where the physician’s understanding of the pathoanatomy of clubfoot, knowledge of the Ponseti method, and technical skill all play a crucial role. Because this deformity arises as a consequence of inadequate treatment, it cannot be diagnosed prenatally or on ultrasound.
Due to poor-quality treatment, the foot develops additional structural deformities, which give it extra visible features. Physicians sometimes refer to this type of foot as “resistant”, because even after 4–5 casts, the foot not only fails to improve but actually worsens and becomes more difficult to correct.
Children who develop this type of foot often struggle with serious skin problems under the cast: redness, wounds, abrasions, significant swelling, and bruising. These complications further worsen the situation and increase the complexity of the deformity. Poorly applied casts may slip, the foot may slide out or get wedged, the skin becomes stiff as in lymphedema, and the slipping cast can create new deformities or reinforce existing ones.
The risk of soft tissue surgery, which may eventually become necessary, ranges from 3% to 5%.
CHARACTERISTICS
Due to casts frequently slipping off, the foot becomes wedged inside them. This causes the calcaneus to be artificially lifted, resulting in a severe equinus position of 50° to 70°. In some cases, the proximal part of the calcaneus comes into contact with the distal fibula and becomes locked there. As a result, the Achilles tendon becomes extremely tight, thickened, and fibrotic up to the mid-calf. Similarly, the gastrocnemius muscle is reduced in size and volume, concentrated in the upper part of the calf.
The Achilles tendon pulls the calcaneus strongly upward, with the external sign being a deep crease above the heel. The outline and shape of the heel are also altered: it often appears misshapen, flattened, compressed, or tilted. The thick fatty tissue inside the heel makes the calcaneus difficult to palpate, giving the impression that the heel is soft and hollow.
Because all the metatarsal bones are strongly plantarflexed due to an excessively shortened plantar fascia, the foot develops a high arch, and a deep transverse crease forms on the sole. It gives the appearance as if the foot were “broken in half.” At the same time, the foot becomes noticeably shorter (for example, in unilateral cases, the affected foot may be 1.5–2 cm shorter than the healthy one).
A large amount of fatty tissue accumulates on the dorsum of the foot, giving the impression that the foot is permanently swollen. This makes it difficult to properly grasp the foot before performing manipulation and applying a cast, as the foot is short and the fatty tissue is dense.
Plantar positioning of the metatarsal bones and an excessively shortened plantar fascia, according to the Hicks mechanism, cause the big toe to be excessively extended upward (hyperextension). As a result, it appears to be “pushed” deep into the foot, and the first ray becomes shortened.
WIDNDLASS MECHANISM
When the plantar fascia is shortened, the big toe automatically goes into hyperextension because the longitudinal arch of the foot is abnormally elevated, pulling the metatarsal bones toward the calcaneus. The elevated longitudinal arch pulls on the extensor tendons of the big toe, which in turn pull the toe upward.
TREATMENT
“GROTUESQUELY DEFORMED FOOT”
Treatment with the Ponseti method is highly effective, allowing feet to regain full functionality and a normal appearance. This high success rate and relative ease of treatment applies to the vast majority of clubfeet. However, some cases are resistant to standard manipulation and casting — namely, atypical and complex clubfeet.
As early as 1994, Dr. Vincent J. Turco noted that these feet “respond very differently to operative and non-operative treatment, and early surgery leads to a grotesquely deformed foot.” He was the first to describe them as “atypical clubfoot” and advised against any surgical intervention on such feet.
In 2006, Dr. Ignacio Ponseti and his colleagues reported changes to the standard treatment protocol, introducing a modified Ponseti protocol for these cases.
In this modified protocol, both the manipulation techniques performed before casting and the casting process itself differ from the classical approach. After the necessary tenotomy, plaster casts may need to be changed more frequently than in standard treatment. The use of the abduction brace is also adjusted — including its wear schedule, positioning, and even the type of brace used.
The key element of this treatment protocol is the very precise localization of the talar head and strict adherence to the individual steps carefully described by Dr. Ignacio Ponseti.
The deformity is difficult to treat because, although forefoot adduction can usually be corrected after the first or second manipulation and casting, the metatarsal bones remain rigidly plantarflexed, and the calcaneus remains fixed in an equinus position. Additional attempts to correct hindfoot varus by abducting the foot result in over-abduction of the strongly plantarflexed metatarsals. Because of the rigid and severe equinus of both the calcaneus and the metatarsals, casts slip easily, which worsens the deformity and damages the swollen skin on the dorsum of the foot. To correct hindfoot varus in complex clubfoot, the hindfoot must be abducted while counterpressure is applied not only on the head of the talus but also on the lateral malleolus. The forefoot should not be abducted beyond its normal alignment. Once hindfoot varus is corrected, the plantarflexed forefoot and valgus deformity can be corrected simultaneously by forcefully dorsiflexing the metatarsals with both thumbs while applying a reinforcing plaster cast.
Let us now take a closer look at each step to make the treatment process clearer.
STEP 1 – 30°–40° AND NO MORE: CORRECTING ADDUCTION
In the standard treatment protocol consistent with the principles of the Ponseti method, applying counterpressure to the talus from the lateral side and slowly abducting the foot in supination allows free movement of the calcaneus, thereby achieving correction.
However, in atypical and complex clubfeet, this maneuver cannot be used. It would cause excessive abduction of the forefoot at the Lisfranc joint and even greater plantarflexion of the metatarsals and toes. This is due to the shortened and tight deep plantar muscles. A visible sign of such an incorrect maneuver is a deep crease along the lateral border of the foot.
To ensure the correct position of the talar head during manipulation (and later when applying the plaster cast), the index finger should rest on the posterior aspect of the lateral malleolus, while the thumb of the same hand applies counterpressure to the lateral side of the talar head — not to the prominent anterior tuberosity of the calcaneus. To avoid abduction at the Lisfranc joint, only 30°–40° of abduction is allowed — and no more! Forefoot adduction is usually corrected easily after one or two manipulations and the application of one or two plaster casts in the position described above, changed weekly.
STEP 2 – SIMULTANEOUSLY: CORRECTING METATARSAL FLEXION AND EQUINUS
After achieving 40° of foot abduction, the method of manipulation must be changed, because the metatarsal bones remain in strong plantarflexion and the hindfoot remains in severe equinus. The aim of this adjustment is to simultaneously correct both the plantarflexion of the metatarsals and the severe equinus of the calcaneus.
For this purpose, both index fingers should be placed on either side of the talar head, with the thumbs positioned on the first and fifth metatarsal heads (“four fingers” technique). An assistant holds the leg with the knee flexed. The physician then slowly lifts all the metatarsals toward a neutral position, while allowing the trapped calcaneus to move out from under the talus. Care must be taken not to over-abduct either the metatarsals or the hindfoot.
The manipulation focuses on stretching the tightly contracted plantar fascia and the tendons of the plantar and medial side of the foot.
CASTS
A complex clubfoot develops as a result of improper casting — the casts are poorly molded, often slip off, the foot becomes wedged inside, swelling occurs, fatty tissue shifts into certain areas, and bruising appears. Applying another cast on such a foot only creates additional deformities and makes them permanent. The first step is to remove a slipping cast immediately! The second step is… to change the doctor.
Before restarting treatment and recasting, it is essential to allow time for the swelling in the leg and foot to subside. Casting a swollen foot and leg is pointless and only leads to further complications. Sometimes the break from casting may be long. The foot may return to its faulty original position, but this is actually better before resuming treatment than applying plaster casts over swelling.
A full cast is applied, extending from the toes to the groin, exactly as in the standard Ponseti protocol. However, to prevent the cast from slipping off a stocky foot, the leg should be bent at the knee at 110–120° (not 90°) during casting, and the cast applied in this position.
The cast is additionally reinforced: a plaster splint is applied to the calf, heel, and sole, and then fully wrapped with plaster. This helps avoid excess plaster in front of the ankle joint. A small plaster splint is also placed over the front of the knee, then fully wrapped, to prevent excess plaster behind the knee. The cast at the front of the thigh may be gently flattened at the top, while the talar region and foot are carefully molded.
The toes should rest on a stable plaster platform beneath them. Without this support, the already overactive plantar flexors act even more strongly. The platform stretches them evenly and effectively disengages the Hicks windlass mechanism, contributing to correction of the cavus deformity and excessive hallux hyperextension. All toes should remain visible, side by side, in one line — not curled, not overlapping. However, they should not be left exposed, as is standard in the Ponseti method, because in this case it is necessary to secure the big toe to prevent it from being excessively extended.
Typically, 5–8 plaster casts are sufficient to correct the deformity (with exceptions in more difficult cases, e.g., clubfoot in children with arthrogryposis).
STEP 3 – PERCUTANEOUS ACHILLES TENDON TENOTOMY
A percutaneous Achilles tendon tenotomy is necessary in almost all cases. It is performed once the physician has achieved slight abduction of the foot (up to about 30°) and correction of excessive plantarflexion of the metatarsals, while equinus persists (the equinus deformity is not fully corrected). An earlier tenotomy may be required if the cast slips off too frequently or if the foot is so deformed that the calcaneus is locked near the fibula in severe plantarflexion, preventing any movement and making it impossible to achieve 30° of foot abduction.
The tendon is cut approximately 1.5 cm above the crease visible above the heel. This distance helps avoid injury to the posterior tuberosity of the calcaneus, which is positioned very high due to the severe equinus deformity. To achieve correction, at least 10° of dorsiflexion is required. If this is obtained during the procedure, the final cast is applied for 3–4 weeks in a maximum of 40° of abduction.
When 10° of dorsiflexion cannot be achieved during the procedure due to severe equinus of the calcaneus, the casts are then changed weekly (from one to four times) until both abduction of the foot (up to 40°) and dorsiflexion (at least 5°, preferably 10°) can be obtained.
STEP 4 – FOOT ABDUCTION BRACE
Parent education is key when it comes to the effective use of the abduction brace, which is applied immediately after the cast is removed following percutaneous Achilles tendon tenotomy.
The shoes must be carefully made and properly fitted to prevent the feet from slipping out, and the foot abduction brace must be correctly adjusted. The Mitchell brace provides this level of security. The standard Denis Browne bar with lace-up shoes is not sufficient for this type of foot: the foot often slips out, losing correction. It is also difficult to control heel position inside the shoe — which is critical.
The initial brace setting should be 20°–40° of abduction (studies show varying values, though 40° is most common), depending on whether the foot is atypical or complex. Later, as the foot begins to take on a near-normal shape, abduction may be increased to 50°, and should then be gradually increased every few weeks until reaching 60°.
The brace is used until the age of 5 years to prevent relapse.
TECHNIQUE-NOT THE FOOT
Very often, a typical, standard clubfoot is turned into a complex clubfoot because of poor casting. In such cases, many parents are told: “This foot is difficult, uncorrectable, stiff” — and that surgery will surely be needed because the doctor cannot achieve correction.
Many physicians are not even aware that they are creating such feet. They frequently dismiss this type of deformity, telling parents: “You took poor care of your child, you carried them wrong, and that’s why the cast slipped or fell off.”
THIS IS NOT TRUE!
Transforming a standard clubfoot into a complex clubfoot is never the fault of the foot itself — it is ALWAYS the result of poor casting technique.
THE RISK OF RELAPSE
In atypical and complex clubfeet, the relapse rate is as high as 68%, and unlike in standard clubfoot, it does not decrease with prolonged use of the abduction brace. This is a significant figure, and families must be prepared for different scenarios. Unfortunately, to date, no studies have distinguished relapse risk separately for atypical versus complex clubfeet.
Nevertheless, despite this high risk of relapse, treatment with the Ponseti method in children aged 4–10 years yields very good results in the early stages, significantly reducing the need for invasive surgery. In some cases of relapse, repeating proper casting or performing a simple procedure such as anterior tibial tendon transfer (ATTT) or a minimally invasive percutaneous triple hemisection (Hoke’s technique) can be effective alternatives to invasive surgeries, such as extensive releases — including posteromedial release. Dr. Vincent J. Turco himself stated that such releases create an additional problem: overcorrection leading to a rigid flat-valgus foot. The earlier such surgeries are performed, the more severe the deformity becomes, resulting in lifelong complications that may not be immediately apparent but develop over time.
In general, there is no need for extensive surgical interventions, since using the modified Ponseti method provides excellent outcomes, even in cases of relapse. When relapse does occur, the standard procedure is simply to return to casting, as described in the article on RELAPSES.
WORDS OF HOPE
Although atypical and, even more so, complex clubfoot are specific examples of deformity, the modified Ponseti method is a safe and effective treatment with excellent long-term results, drastically reducing the need for any surgery — including invasive procedures such as posteromedial release (PMR).
The shape, length, and dorsiflexion of the foot improve within a few months after correction. In addition, the motion of the subtalar joint also normalizes, and over time the foot develops properly, allowing your child to be fully functional.
MEDICAL RESEARCH & MEDICAL SOURCES
- Ponseti I.V.: „Congenital Clubfoot. Fundamentals of treatment.” (2nd edition)
- Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Turco V.J.: „Recognition and Management of the Atypical Idiopathic Clubfoot”, Springer-Verlag New York, Inc. 1994
- Gupta A. et al.: „Atypical clubfoot: Early Identification and treatment by modification of standard Ponseti technique.”
- Dobbs M.B., Williams M.: “Congenital Foot Deformities.” | “Pediatric Lower Limb Deformities. Principles and Techniques of Management.” (2nd etition)
- Masquijo J., Arana E.: “Complex clubfoot: my 5 tips for appropriate evaluation nd treatment with the Ponseti method.”
- Chu A. et al.: “Management of complex clubfoot.”
- Rangasamy K. et al.: „Correction results of atypical clubfeet managed with modified Ponseti technique: A meta-analysis of 354 feet.”
- Allende V. et al.: „Complex clubfoot treatment with Ponseti method: a Latin American multicentric study.”
- Yadav A. et al.: „Management of complex idiopathic clubfoot using modified Ponseti method.”
- Rodrigues N. et al.: „Management of Complex Clubfoot: Challenges and Solutions”
- Agarwal A. et al.: „Results of Modified Ponseti Technique in Difficult Clubfoot and a review of literature.”
- Matar H.E. et al.: „Treatment of complex idiopathic clubfoot using the modified Ponseti method: up to 11 years follow-up.”
- Bozkurt C. et al.: „Using the modified Ponseti method to treat complex clubfoot: Early results.”
- Radler C., Herzenberg J.E. et al.: „Ponseti versus traditional methods of casting for idiopathic clubfoot.”
- Ponseti I.V., Morcuende J.A. et al.: „Radical reduction in the rate of extensive corrective surgery for clubfoot using the Ponseti method.”
- Bolgla L.A., Malone T.R.: „Plantar Fasciitis and the Windlass Mechanism: A Biomechanical Link to Clinical Practice.”
- Loose O. et al.: “Complex, atypical clubfoot: follow-up after up to 16 years reveals a high risk of relapse but good functional and radiological outcomes”
- Radler C.: “Standard AFO for clubfoot and atypical clubfoot a unified approach.”
- Morcuende J.A.: “Complex Clubfeet: Recognition & Management.”
- Morcuende J.A.: “Pediatric Orthopedics Active learning Session – Management of Relapsed Clubfeet : Dr Jose Morcuende”
- Ponseti International Association (Ponseti I.V.): “Complex Clubfoot at Birith”
PHOTOS & GRAPHICS
In the order of appearance on the page:
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- 1-3: Own
- Windlass Mechanism
- Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Redressions: Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- Redressions: Ponseti I.V. et al.: “Treatment of the complex idiopathic clubfoot.”
- 8-12: Own