Congenital clubfoot is a common deformity, the incidence of which is reported to be as high as 1‰ to 3‰ abroad and is also common in China. It is more common in males than females, and more bilateral than unilateral. Some cases have a family history. The disease may exist alone or may be accompanied by other deformities, such as spina bifida, hip dislocation, polydactyly, and syndactyly. The disease includes four factors of deformity: pronation of the foot, ankle plantar flexion, forefoot inversion and internal rotation of the tibia. It can be detected immediately after birth, thus the diagnosis is not difficult. However, the etiology, pathology and pathogenesis of the disease have not been fully understood, so the principles of treatment and treatment methods have not been unified. If it is treated early and appropriately, most of the results can be satisfactory, but if it is not treated, it will be crippled for life and affect life and work. There are many theories about the etiology of this disease, such as genetic theory, abnormal development of primitive bone matrix, soft tissue contracture of the foot, vascular anomalies, neuromuscular anomalies, regional growth disorders, and in utero developmental blockage theory. However, in recent years, there is a tendency to advocate that the disease is related to abnormal neuromuscular developmental lesions. It is believed that congenital clubfoot is the result of muscle imbalance in early fetal life, and the alteration of muscle strength is based on neurological abnormalities. Skeletal, joint and soft tissue contractures are adaptive changes secondary to muscle imbalance. It was found that the ratio of type I to type II muscle fibers in the posterior and medial calf muscles was deranged, with an increase in type I muscle fibers and aggregation, which was seen in denervated areas. Degenerative and regenerative changes of nerve fibers and motor endplates were also found. With the development of the deformity, the development of each muscle was affected, with contracture of the anterior tibial and posterior tibial muscles, and the peroneal muscle was thin and in a state of passive pulling and lengthening due to prolonged inversion of the foot, and its muscle strength and external rotation were gradually reduced. Some scholars examined the affected dead infant and found that the weight of the affected peroneal muscle was only half of that of the healthy side. The muscle strength imbalance is a common clinical phenomenon, i.e. the inversion muscles (anterior tibial and posterior tibial muscles) are strong and short, while the extensor muscles (peroneal muscles) are weak and elongated, forming an imbalance between the inversion and extensor muscles; at the same time, the plantar flexor muscles (triceps calf) are stronger than the dorsal extensor muscles (anterior tibial muscles), forming a typical horseshoe foot deformity. The pathology of this disease involves both soft and skeletal tissues. In newborn infants, most of them have only soft tissue changes and normal or only slight bone and joint changes, but the lesions may progressively worsen with age. The ligaments, tendons and fascia of the foot and ankle become shorter and contracted, with the posterior medial calf muscle and plantaris muscle being the most obvious, while the peroneal muscle and foot extensor muscle are elongated and relaxed. Sometimes the Achilles tendon, anterior tibial muscle, posterior tibial muscle or peroneus brevis tendon stops are abnormal. In a few cases, the anterior tibial muscle is dysplastic. The joint capsule of the medial and posterior part of the foot is contracted, and the medial and metatarsal ligaments of the foot, such as the medial deltoid ligament, heel navicular ligament, spring ligament, and the posterior heel fibular ligament and talofibular ligament, are contracted. Bony changes are mainly in the tarsus. The talus is deflected medially and metatarsally, the heel bone is internally displaced, the navicular bone is internally displaced, and the talofibular joint is dislocated. The dice bone is internally displaced, near the medial aspect of the distal heel bone. In advanced patients, metatarsal inversion and tibial internal rotation are seen. Second, clinical manifestations and diagnosis Since the foot deformity can be seen after birth, it is usually not difficult to diagnose. Congenital clubfoot can be divided into stiff type (endogenous type) and floppy type (exogenous type). 1.Stiff type The deformity is severe. The ankle and subtalar joint plantarflexion deformity is obvious, the talus is plantarflexed, and the protruding talar head can be felt under the skin from the dorsal side of the foot. Because the posterior end of the heel bone is upturned and hidden in the posterior side of the lower tibia, the heel seems to become smaller, and at first glance it appears to be stick-shaped without a heel, so it is also called stick-shaped foot. The Achilles tendon is severely contracted. From the posterior side, the heel bone is turned inward. The forefoot is also inwardly turned inward, with the navicular bone located deep in the medial aspect of the foot, near the talar head, and the dice bone protruding toward the lateral aspect of the foot, with the medial aspect of the foot concave. The medial ankle and medial heel skin lines increase, while the lateral and dorsal skin of the foot is stretched and thinned. The deformity is not easily corrected because it is rigidly fixed when the passive dorsal extension is turned out. The child has difficulty standing, delayed walking, and limping, and the lateral or dorsal aspect of the foot is seen when supporting standing. At an older age, the limp is obvious, the soft tissues and joints are stiff, the foot is small, the calf is thin, and the muscle atrophy is obvious, but the sensation is normal. Thickened bursa and callus can appear on the lateral side of the dorsal foot after long-term weight bearing, and the foot is severely deformed. 2, flabby type The deformity is lighter, the size of the heel is close to normal, the calf muscle atrophy thinning is not obvious. The most important feature is that the horseshoe deformity can be corrected during passive dorsal extension and valgus, and the affected foot can reach or approach neutral position. This type of deformity is more floppy, easy to correct, easy to consolidate, not easy to recur, and has a good prognosis. This type is due to abnormal intrauterine position. The diagnosis of this disease can be made based on clinical manifestations, and generally does not need to be confirmed based on x-ray examination. However, radiographs are indispensable for judging the degree of horseshoe and entropion deformity and for objective evaluation of the treatment. In the orthopantomograph of a normal foot, the extension of the long axis of the talus reaches the 1st metatarsal via the navicular bone and cuneiform bone, while the extension of the long axis of the heel reaches the 4th metatarsal, with the two lines intersecting at an angle of 20-40° (heel-distance angle); in the lateral view, the long axis of the talus intersects with the long axis of the heel at an angle of 35-50° (heel-distance angle). The orthopantomogram of the clubfoot shows that the heel and talus are superimposed on each other, and both are facing the 5th metatarsal, and the heel talus angle is reduced or disappears; after 3 years of age, the navicular bone ossifies and the navicular bone is seen to be displaced medially; the lateral film shows that the heel talus angle is <35°, usually 20° or less. The sum of the orthogonal and lateral heel spur angle values is the heel spur index. The disease should be differentiated from the following diseases: a. Spina bifida is palpable in the lumbosacral region with spinous process agenesis or spondylolisthesis, which can be determined by radiographs if necessary. It is often associated with neurological damage, such as loss of sensation in the feet, motor impairment, and even urinary and fecal dysfunction. b. Polyarticular contracture, in which joint stiffness is present after birth, is difficult to correct by manipulation and involves more joints. c. Post-polio paralysis, with its history of onset, good sensation and loss of motor function. d. Cerebral palsy, which is spastic paralysis, with increased muscle tone, hyperactive tendon reflexes, and pathological reflexes, often with intellectual deficits.