Knowledge about congenital clubfoot

  Congenital clubfoot
  I. Overview.
  Congenital clubfoot is one of the three major congenital malformations in pediatric orthopedics, incidence: 1 per 1,000 ; male: female = 5:1 
  Second, the etiology: multifactorial cause.
  (a) genetic theory: the population incidence of 1‰, the first generation of congenital clubfoot, the offspring incidence of 2.9%, 29 times higher than normal, 39% of relatives of the same generation each disease; chromosome 6, 11, 18, bit gene mutation, may be the causative gene.
  (B) neuromuscular lesions (the focus of current research)
  Some studies have found denervated neuromuscular changes in the gastrocnemius muscle and atrophy of the calf muscle. In our study, we found atrophy of the calf muscles on ultrasound.
  (iii) Genetic mutations
  Genes regulate the formation of limb germ during embryonic development
  (iv) Fibrous tissue contracture
  Contracture of the metatarsal fascia, joint capsule ligaments, and Achilles tendon.
  (v) Abnormal embryonic skeletal development
  The main abnormalities are talus, heel bone, navicular bone, and morphology. In our study, we found that the abnormal relationship of tarsus is also one of the causes of congenital clubfoot.
  Classification
  According to the etiology, there are three clinical categories
  1. Postural clubfoot
  Soft, due to intrauterine fetal position in late pregnancy, the deformity is quickly corrected by a series of plaster orthopedic, without the need for Achilles tendonotomy.
  2. Idiopathic clubfoot
  The degree of stiffness is moderate, due to the synergy of multiple factors.
  3. Deformed clubfoot
  It is often accompanied by joint contracture, spinal cord spondylolisthesis and other systemic diseases, with severe stiffness, which is difficult to treat.
  IV. Clinical manifestations
  Forefoot ptosis (ankle plantarflexion).
  Forefoot inversion.
  Internal rotation of forefoot (inversion of the foot).
  Internal rotation of the lower leg, significant muscle atrophy, and normal muscle strength.
  From the clinical treatment effect observation, there are 2 types
  1. Rigid type
  Severe and fixed, with obvious horseshoe, inversion and inversion deformity, mostly bilateral.
  2. Floppy type
  The deformity is mild, the skin and tendons are asymmetrical, and can be corrected by manipulation.
  V. Diagnosis
  Diagnosis based on the typical foot deformity after birth, joint stability and can grow with age, standing and walking, and normal muscle strength.
  X-ray examination.
  Orthopantomograph: normal talus a navicular bone – cuneiform bone in a straight line with the heel bone dice bone fourth metatarsal another straight line intersection 30 ~ 35 °; abnormal for 10 ~ 15 °; abnormal for 10 ~ 15 °.
  35°; abnormal is 10-15°.
  Lateral radiograph: the angle of intersection between the normal talus and the axis of the heel bone is 30° (heel distance angle); abnormal is 5-10°.
  VI. Treatment
  Principle: Early diagnosis, early treatment.
  (I) Non-surgical treatment: (<6 months)
  1. Manipulation correction: <1 month, flaccid type , good results.
  2. Plaster correction; >1 month, stiff type, prepare for surgical correction, change the plaster once a week, perform closed Achilles tendon cut after 4-5 casts, remove the plaster three weeks after surgery and switch to brace treatment.
  (ii) Surgery For children who missed conservative treatment or failed conservative treatment.
  Methods
  1. early muscle balancing surgery, soft tissue release
  2. tendon transposition
  3. Turco surgery
  4. Mckay surgery
  5. Carroll surgery
  6.Triple joint fixation, age >12 years