1. CLUB FOOT (Talipes equinovarus)

2. Posturing is the habitual position in which the infant holds the foot;passive range of motion is normal.
Deformity produces an appearance similar to posturing but passive motion is restricted
most pediatric foot disorders are painless,pain is more common in older children.

3. Definition
Rigid congenital deformity of the foot,consisting of hindfoot equinus, hindfoot varus, and forefoot varus.
clubfoot deformity involves the entire leg,not just foot.
the tarsals in the affected foot are hypoplastic;the talus is most affected.
The muscles of the limb are hypoplastic because of the abnormal tarsal interactions,which leads to generalized limb hypoplasia,mainly affecting and shortening the foot. There is usually atrophy of the calf musculature.
affects 1 in 1000 newborns and is bilateral in 50% of cases.
more in boys.
Incidence in first-degree relations is approximately 2%.
Incidence in second-degree relations is approximately 0.6%.

5. clinical manifestations
The infant will have :
hindfoot equinus and varus.
forefoot adduction.
varying degrees of rigidity.
all are secondary to the abnormalities of the talonavicular joint.
calf atrophy and foot shortening are more noticeable in older children.
cavus of the foot(high arch foot)
internal rotation of the leg.
The heel is small and empty,feels soft to the touch

6. pathophysiology Arrest of fetal development in the fibular stage.
Theories of the pathogenesis of clubfeet:
Arrest of fetal development in the fibular stage.
Defective cartilaginous anlage of the talus.
Neurogenic factors.
Retracting fibrosis.
Anomalous tendon insertions.
Seasonal variations.

7. Etiology congenital (75%).
teratologic;associated with a neuromuscular disorder (as myelomeningocele,arthrogryposis).
positional:normal foot that was held in the deformed position in utero.

8. At presentation:
take a detailed family history of clubfoot or neuromuscular disorders.
perform a general examination to identify any other abnormalities.
Examine the feet with the child prone, with the plantar aspect of the feet visualized, and supine to evaluate internal rotation and varus.
If the child can stand, determine whether the foot is plantigrade, whether the heel is bearing weight, and whether it is in varus, valgus, or neutral.
examine for myelomeningocele and arthrogryposis.

9. evaluation
doctors can see it on ultrasound images taken after about 4 months of pregnancy.

10. radiologic evaluation
rarely necessary for assessment because their tarsals have incomplete ossification.
navicular ossifies at about 3 years of age for girls,4 years for boys.
as children age radiographs can be used to follow the tibial calcaneal and lateral talocalcaneal angles and to assess navicular positioning.

11. 1) abnormally elevated tibiocalcaneal angle. A normal angle is 60-90°.
2) lateral view shows the nearly parallel talus and calcaneus talocalcaneal angle <25 , normal is between 25 and 45.
1) abnormally elevated tibiocalcaneal angle. A normal angle is 60-90°.

12. Dorsoplantar view how that the talus and calcaneus are more overlapped than in the normal condition. The talocalcaneal angle <15°,normal 15-40°. 12

13. Dorsoplantar view shows that the convergence of the bases of the metatarsals is abnormally increased compared with the normal convergence.
8/2/2018

14. Treatment:
If the condition is not corrected early, secondary growth changes occur in the bones and these are permanent.
Relapse is common, specially in babies with associated neuromuscular disorders and if parents had club foot…
Nonsurgical treatments such as casting (plaster of Paris )or splinting are usually tried first. The foot is moved (manipulated) into the most normal position possible and held (immobilized) in that position until the next treatment. 
This manipulation and immobilization procedure is repeated every 1 to 2 weeks for 2 to 4 months (or depending on the case, maybe just stop after two casts) , moving the foot a little closer toward a normal position each time. Some children have enough improvement that the only further treatment is to keep the foot in the corrected position by splinting it as it grows.
The two common methods of manipulation and casting are the "traditional" and the Ponseti (Iowa) methods.

15. Treatment cont…
If a few months of progressive manipulation and immobilization don't move the foot into a more normal position,may suggest surgery. 
The most common surgical procedures are to lengthen or release the tight soft-tissue structures, including ligaments and tendons and to reposition the bones of the ankle as needed. Small wires are often used to hold the bones in place and then are removed after 4 to 6 weeks. Splinting or casting is usually used after surgery to keep the foot in the correct position during healing.
After that, hobble boots (Denis Browne) or customized orthosis are used to maintain the correction.
A mild recurrence of clubfoot is common, even after successful treatment. Also, the affected foot will continue to be somewhat smaller (often 1½ shoe sizes or less) and stiffer than the unaffected foot, and the calf of the leg will be smaller. But after treatment most children are able to wear shoes comfortably and to walk, run, and play. If child is not walking by the time he or she is 18 months old,make sure that child doesn't have another health problem. 15

16. 8/2/2018

17. Flat Foot
Definition : is a postural deformity in which the arches of the foot collapse, with the entire sole of the foot coming into complete or near-complete contact with the ground. 17

18. 18

19. There is a functional relationship between the structure of the arch of the foot and the biomechanics of the lower leg. The arch provides an elastic, springy connection between the forefoot and the hind foot .
This association safeguards that a majority of the forces incurred during weight bearing of the foot can be dissipated before the force reaches the long bones of the leg and thigh . 19

20. In Flat foot the head of the talus bone is displaced medially and distal from the navicular. As a result, the spring ligament and the tendon of the tibialis posterior muscle are stretched, so much so that the individual loses the function of the medial longitudinal arch (MLA). 20

21. Etiology Family history
The feet bones not forming properly in the womb (tarsal coalition)
loose connective tissue throughout the body, such as in Ehler-Danlos syndrome or Marfan’s.
a condition affecting the muscles and nerves, such as CP, spina bifida or muscular dystrophy.
Accessory navicular
Tarsal coalition: The small bones of the foot (tarsals) do not separate properly during development 21 21

22. Benign (Flexible) flat foot
It appears in toddlers as a normal stage in development often due to the thick subcutaneous plantar fat pad and joint laxity.
the MLA is present and functional while the individual is sitting or standing up on their toes, but this arch disappears when assuming a foot-flat stance.
It usually disappears after a few years when the development of the median arch is complete .
Many of the children with flexible flat foot have ligamentous laxity (loose ligaments), and there might be a family history of both flat feet and joint hypermobility . 22

23. The parents notice that the feet are flat or the shoes wear badly
Clinically:
Flexible flat-foot:
No symptoms
The parents notice that the feet are flat or the shoes wear badly
The deformity becomes noticeable when the child stands.
On examination:
Ask the patient to go up on tiptoes: if the heels invert, it is a flexible deformity.
Then examine the foot with the child sitting or lying.
Feel for localized tenderness
Test the range of movement in the ankle, subtarsal & midtarsal joints.
A tight Achilles tendon may induce a compensatory flat-foot deformity. 23

24. The arches are reconstructed and the heels go into mild varus when the child is on tip-toes.24

25. Pathological (stiff ) flat foot
It ocurs in older children and adolescence .
the MLA is absent or nonfunctional in both the seated and standing positions
It cannot be corrected passively and it should alert the examiner for and underlying abnormality (congenital mal alignment, neurological or muscular diseases, arthritis, bones coalition, tendon injuries) 25

26. Clinically:
Stiff flat foot presenting with pain, particularly in the heel or arch area. Pain may worsen with activity. Swelling along the inside of the ankle can also occur.
On examination:
The peroneal and extensor tendons appear to be in spasm, sometimes its called “Spasmodic flat-foot”
The spine, hips & knees should always be examined as well as joint hypermobility and neuromuscular abnormalities.
In some cases a definite cause may be found, but in many no specific cause is identified. 26

27. 27

28. Imaging
X-rays : this kind of imaging is unnecessary for asymptomatic flat-feet and flexible flat-feet . But we do use it to identify the underlying condition in pathological flat-feet .
Ct-scan : this is the most reliable imaging for tarsal coalitions ( A tarsal coalition occurs when the bones of the feet fail to separate during fetal development ) . 28

29. X-ray images
In normal feet, the relationship between talus and 1st metatarsal results in a straight line being formed along their axis (Meary's angle = 0 degrees). This is not the case in flat feet where there will be:
loss of the normal straight line relationship
sag at the talonavicular joint or naviculocuneiform joint 29 29

30. Treatment Conservative care:
Stretching exercises for the calf and hamstring muscles
Physiotherapy to strengthen muscles and improve coordination
Orthoses (Insoles), ankle braces
Anti inflammatories and analgesics
Local steroid injections
Supportive shoes 30

31. Surgical treatment:
This involves a combination of techniques to restore alignment of the foot to the lower leg and includes osteotomies (cutting bones to re-align them), fusing joints(triple arthrodesis) , tendon lengthening and transfers as well as implanted devices to help maintain correction
Triple arthrodesis is a surgical procedure whose purpose is to relieve pain in the rear part of the foot, improve stability of the foot, and in some cases correct deformity of the foot, by fusing of the three main joints of the hindfoot: the subtalar joint, calcaneocuboid joint and the talonavicular joint. 31 31

32. 32

33. خلع الورك التطوري

34. Simple Anatomy
The hip is a “ball-and-socket” joint that is held together by ligaments (ligament of teres, ileofemoral, ischiofemoral, transverse ligament) The ball is called the “femoral head” which is the top of the femur or thigh bone. The socket is called the “acetabulum” and is a part of the pelvis. The femoral head fits into the acetabulum creating the hip joint. This joint is normally held tightly in place by the surrounding ligaments and joint capsule.

37. Nerves:
Femoral nerve in front
Sciatic nerve in back of the hip
Obturator nerve
Blood Vessel:
Femoral artery has a deep branch, called the profunda femoris, which sends 2 vessels that go through the hip joint capsule.
Lateral & Medial femoral circumflex arteries main blood supply for the femoral head, ligamentum teres (Ligament of the head of the femur) contains a small blood vessel hat gives a very small supply of blood to the top of the femoral head.

38. Definition of DDH:
The old term for such condition used to be congenital dislocation of the hip (CDH), which now has been replaced by developmental dysplasia of the hip (DDH) because the latter is more representative and encompasses the spectrum of abnormalities seen in this condition. The term CDH tends to refer to a defect where something is missing or added to normal tissues when born. In the case of DDH, the infant/child’s joint is otherwise normal except for the instability, leading to abnormal growth of the hip joint.
So, DDH is a congenital (Teratological forms of mal-articulation) or acquired (at birth); deformation or misalignment of the hip joint, the hips are usually not dislocated but rather “dislocatable”. And it’s the medical term for general instability, or looseness, of the hip joint.
The term DDH also describes the range and evolution of abnormalities that occur in this condition.
It is NOT a one step disease !!

39. The primary stimulus for growth and development of the hip joint comes from the femoral head being accurately located in the acetabulum. A possible hypothesis to explain the dysplasia is that the hip will not develop normally unless the head of the femur rotates about a point axis within the acetabulum. If rotation occurs about an eccentric or moveable axis, as in DDH, acetabular development will not proceed normally (Dysplasia).
In acetabular dysplasia the acetabulum (socket) is too shallow or deformed. The center-edge angle is measured as described by Wiberg. Two forms of femoral dysplasia are:
Coxa vara, in which the femur head grows at too narrow an angle to the shaft.
 Coxa valga, in which the angle is too wide.

40. > <1200

41. Types of DDH according to severity:
In all cases of DDH, the socket (acetabulum) is shallow, meaning that the ball of the thighbone (femur) cannot firmly fit into the socket. Sometimes, the ligaments that help to hold the joint in place are stretched. The degree of hip looseness, or instability, varies among children with DDH.
Dislocated. In the most severe cases of DDH, the head of the femur is completely out of the socket.
Dislocatable. In these cases, the head of the femur lies within the acetabulum, but can easily be pushed out of the socket during a physical examination.
Subluxatable. In mild cases of DDH, the head of the femur is simply loose in the socket. During a physical examination, the bone can be moved within the socket, but it will not dislocate.

42. 1) The condition could be bilateral or unilateral:
If both hip joints are affected one speaks of "bilateral" dysplasia. In this case some diagnostic indicators like asymmetric folds and leg-length inequality do not apply.
In unilateral dysplasia only one joint shows deformity, the contra lateral side may show resulting effects. In the majority of unilateral cases the left hip has the dysplasia.
Left joint (45%) is more common than right joint (20%)
Bilateral dysplasia (35%) is more common than having right hip dysplasia. Left > bilateral > right
2) Not all hip dislocations are present birth, but they all occur before 3 months of age.

43. Pathophysiology
Capsular laxity is the dominant feature in the unstable hip and the tight fit between the femoral head and acetabulum is lost. The femoral head can be made to slide in and out of the acetabulum.
Children often have ligamentous laxity at birth, yet their hips are not usually unstable; in fact, it takes a great deal of effort to dislocate a child's hip. Therefore, more than just ligamentous laxity may be required to result in DDH

44. Pathologic Developments vs. Findings in DDH:
At birth:
The capsule is stretched, lax & redundant.
During infancy, changes in:
Femoral head: dislocated superolateraly to the acetabulum, normal in size, bony nucleus appears late and its development is delayed.
Acetabulum: ossified nucleus is delayed in development, shallow and slopes upward.
Inverted labrum: folded into the acetabulum and is called limbus.
Capsule and ligaments:
Ligamentus teres: elongated and thickened
Transverse ligament of acetabular notch: is pulled up and narrows the entrance to the acetabulum.
The pelvifemoral muscles: shortened esp. hip adductors & iliopsoas muscle, presses on the capsule anteriorly → hourglass appearance.
The muscles get shorter because of their fibrosis resulting from their disuse.
Last 3 points form the main obstacles to reduction of the dislocated hip.

46. Risk factors of DDH:
Hip dysplasia is considered to be a multifactorial condition, and these factors are:
And There are NO definite causes !!
1) Hereditary Factors:
Family history of DDH: (12 times more likely with +ve family history)
If a child has DDH, the risk of another child having it is 6% .
If a parent has DDH, the risk of a child having it is 12% .
If a parent and a child have DDH, the risk of a subsequent child having DDH is 36%
Generalized joint laxity (Dominant Trait)
Shallow Acetabulum (Polygenic Trait)
** Patients with such traits are more likely going to develop bilateral hip dysplasia.
*** These conditions involve genetic mutations, while the points mentioned above in (a) don’t.
Gender: Females are more likely to develop DDH than males (8:1)
Ethnicity: Native Americans and Laplanders have very high prevalence of DDH, while the prevalence is very low in southern Chinese and Black populations.

47. 2) Acquired Factors:
Traditions in nursing the newborn:
In those societies where it is usual to nurse the child with the legs bound together in adduction, the incidence of established DDH is much higher than in those societies where the child is carried on the mother ’ s back with the legs widely abducted.
b) Intrauterine position:
The positioning of the baby in the womb can cause more pressure on the hip joints, stretching the ligaments. It’s thought that babies in a normal position in the womb have more stress on the left hip than on the right hip (position of the left hip against mother’s sacrum). This may be why the left hip tends to be more affected. Babies in the breech position are more likely to have hip instability than babies in a normal womb position.
Normal Womb Position Abnormal Womb Position

48. Picture showing how a papoose board (or cradleboard) is used
Picture showing how a papoose board (or cradleboard) is used. The child’s legs are kept adducted, extended, and tied down tightly by the wrap on the board.
Picture of a mom carrying her child in a back sling. Her babies hips remain spread (wrapped around her mother’s back) keeping the hips is a safe position

49. Oligohydraminos (Deficiency of the amniotic fluid) is also reported to be associated with increased risk for DDH as it causes diminished movement and fetal compression.
Congenital Torticollis: in a shortening or excessive contraction of the sternocleidomastoid muscle, which curtails its range of motion in both rotation and lateral bending.
Large for gestational age: which applies more pressure on the hip joint.
Also, around the time of birth, the mother makes hormones (estrogen, elastin and progesterone )that allow the mother’s ligaments to become lax (stretch easier) so that the baby can pass through the birth canal. Some infants may be more sensitive to these hormones than others, allowing for excessive ligament laxity in the baby.
** The incidence of DDH among premature babies is less than full-term babies because the hormone levels didn’t reach their peak concentration.
g) First born child: (Primagravida)
Has a higher risk for developing DDH, because of the un-stretched uterus and tight abdominal muscles that constrain fetal movement
h) Cerebral Palsy and Myelomeningicele.

50. Signs and Symptoms (noticed by parents)
1) 2) Hip Click: Hip clicks or pops can sometimes suggest hip dysplasia but a snapping sound can occur in normal hips from developing ligaments in and around the hip joint. 3) Limited Range of Motion: Parents may have difficulty diapering because the hips can’t fully spread (During abduction) 4) Pain: is normally not present in infants and young children with hip dysplasia, but pain is the most common symptom of hip dysplasia during adolescence or as a young adult due development of osteoarthritis. 5) Swayback: A painless but exaggerated waddling limp or leg length discrepancy are the most common findings after learning to walk. If both hips are dislocated, then limping with marked swayback may become noticeable after the child starts walking.
Asymmetrical buttock creases: can suggest hip dysplasia in infants but, like a hip click, an ultrasound or x-ray study will need to be done to determine whether the hips are normal or not.

51. Asymmetrical Creases
Swayback Posture

52. Clinical Diagnosis
Clinical findings and investigations (Birth-3 months):
Ortolani maneuver : The classic examination finding is revealed with the Ortolani maneuver, in which a palpable "clunk" is present when the hip is directed in and out of the acetabulum and over the neolimbus. It is a maneuver to reduce a recently dislocated hip through flexion, abduction, anteriorly. ** Only one hip is examined at a time. ** Should be performed gently.
b) Barlow maneuver : another test for DDH that is performed with the hips in an adducted position, in which slight gentle posterior pressure is applied to the hips. A "clunk" should be felt as the hip subluxates out of the acetabulum , Provocative test that attempts to dislocate an unstable hip Flexion ,adduction, posteriorly.

53. Ortolani’s Maneuver
Barlow’s
Maneuver

54. Clinical findings and investigations (>3 months):
c) Asymmetrical buttocks skin folds
d) We cant use X-rays because the acetabulum and proximal femur are cartilaginous and wont be shown on X-ray.
e) Ultra Sound is the best method.
Clinical findings and investigations (>3 months):
a) The Galeazzi sign: is a classic identifier of unilateral hip dislocation (see the image below). This is performed with the patient lying supine and the hips and knees flexed. The examination should demonstrate that one leg appears shorter than the other. Although this finding is usually due to hip dislocation, it is important to realize that any limb-length discrepancy results in a positive Galeazzi sign. (not specific)
c) The most diagnostic sign is limitation of abduction (<600 is almost diagnostic).
d) X-rays after the age of 3 months can be helpful esp. after the appearance of the ossified nucleus of the femoral head
e) US is 100% diagnostic

55. Clinical findings and investigations later in life:
Limping
Waddling gait=bilateral DDH, (Trendelenburg gait= unilateral):
Due to inefficiency of the abductor muscles.
Limitation of hip abduction
Toe-walking
Hyperlordosis
Wide perineum (Bilateral)
An arthrogram: in which radio - opaque dye is
injected into the joint, will show the exact position
and shape of the head and may show the inverted
capsule (limbus)
** HIGH risk groups (presence of congenital anomalies for ex.) undergo special examinations and ultrasonography.

56. Cartilaginous Acetabulum
If the angle shown was <60 then DDH is diagnosed.
Pelvic bone
Bony Acetabulum

57. X-Ray Lines: that are used in identifying a dislocated hip joint
Von Rosen View:
Hips abducted 45º & medially rotated.
We draw a line through the central axis of the femoral shaft.
Normal hip (ossified nucleus) will be inside the acetabulum.
Dislocated hip it will be above acetabulum.
Horizontal Line of Hilgenreiner:
Drawn between upper ends of tri-radiate cartilage of the acetabulum.
Normal hip joint should be below this line.
Vertical Line of Perkins:
Drawn from the lateral edge of the acetabulum vertical to horizontal line.
Normal hip joint should be medial to this line.
4 Quadrants:
Normal hip: the ossification center of the femoral hip lower medial quadrant.
Dislocated hip: upper lateral quadrant.
Acetabular Index:
Angle between horizontal line of Hilgenreiner and the line between the 2 edges of the acetabulum.
Normal hip 20-30º
Dislocated or dysplastic hip ≥ 30º
Shenton’s Line:
Semicircle between femoral neck and upper arm of obturator foramen, in dislocated hip this line is broken.

58. Von Rosen View

60. Management The earlier the better.
Best time for treatment is in newborn period.
It depends on the device and age of the patient.
Goal is to:
Flex and abduct hips.
Reduce femoral head and maintaining it.
To influence the natural growth processes of the baby so a more stable hip joint is developed.

61. 1) Non-Surgical Treatment Methods
These methods are most common when a baby is less than 6 months of age. They typically consist of bracing a baby in such a way so that his or her hips are kept in a better position for hip joint development. The goal is to influence the natural growth processes of the baby so a more stable hip joint is developed.
Pavlik Harness
This is a specially designed harness to gently position your baby’s hips in a well aligned and secure position. This better positioning encourages normal hip joint development over time.
The harness is considered a dynamic reduction method of the hip joint, because the child is able to move his joint in a limited acceptable range of motion.
Hip Abduction Braces
A brace can be used for infants to hold their hips in a properly aligned position to encourage normal hip joint development. Also called fixed-abduction braces, they hold the legs apart and are not flexible like the Pavlik harness. 
Closed Reduction
This is the most common treatment between the ages of 6 and 24 months of age. This is a minimally invasive procedure where the physician physically manipulates the ball of the hip back into the socket. This is done with the child under general anesthesia.

63. 2) Surgical Treatment Methods
The idea of surgery on a young child is enough to worry any parent. However small children have amazing powers of healing. They can re-grow bones to normal lengths and bends will naturally straighten out. The doctors call this “re-modelling” and it is one of the wonders of pediatric orthopedics. If the hip stays in the joint and a complication known as AVN (avascular necrosis) doesn’t happen, then the bones will look completely normal a couple of years after surgery. After most surgical procedures a Spica Cast is used to keep the hip aligned in the new, corrected position while the tissues around the hip joint heal and reform into a proper hip joint. 
The following methods are usually considered after two failed sessions of Spica cast. Spica cast is considered a static reduction of the hip joint, as the child is not able to move his hip joint at all.
Open Reduction
This is done when it is suspected that tissue is keeping the head of the femur (the ball at the top of the thigh bone) from going back into the acetabulum (the socket). In young children, clearing out the hip joint may be all that’s needed. In older children, the ligaments of the hip also need to be repaired.
Pelvic Osteotomy
This is done when the hip socket needs repair. There are several different types of pelvic osteotomy and the choice depends on the particular shape of the socket needing repair and the surgeon’s experience. 
Femoral Osteotomy
This is done when the upper end of the thigh bone needs to be tipped so the ball points deeper into the socket. This is sometimes called a Varus De-rotational Osteotomy (VDO or VDRO)

65. Complications of Treatment
1) Avascular necrosis with excessive abduction 2) Femoral nerve compression with excessive flexion.