Varus deformity of the femoral neck in children. Valgus deformity of the hips in a child

Varus deformity of the neck femur - the basis is the shortening of the neck and a decrease in the cervical-diaphyseal angle. Manifested by limited abduction and rotation of the hip in the hip joint, lumbar lordosis and duck gait. Radiologically, the following deformities are distinguished: congenital isolated, childhood, youthful and symptomatic. Congenital varus deformity is rare.

At newborn shortening of the limb is determined, the greater trochanter of the thigh is located high. In the absence of ossification nuclei, it is difficult to make a diagnosis. When ossification occurs, then a bent neck and shortening of the femoral shaft are found. The distal end of the thigh is shown. The epiphyseal growth zone is located vertically, the femoral head is displaced downwards and backwards, the acetabular cavity is flattened, the greater trochanter is beak-shaped and stands high.

With pediatric varus deformations, which develops at the age of 3-5 years, in the lower medial part of the femoral neck, laterally from the zone of the growth cartilage, a trihedral bone fragment is formed, forming with the upper vertical zone of enlightenment in the region of the head and neck, a picture similar to an inverted letter "U". The course of the fissure is usually tortuous, the bony edges are jagged, uneven, slightly sclerotic.

Later on, the gap expands up to 10-12 mm, the neck is shortened, the head lags behind in development, shifts caudally and approaches the femoral shaft, the greater trochanter is located 4-5 cm above the upper edge of the acetabulum.

juvenile varus deformation is characterized by changes in the growth zone, and not in the bone part of the neck, as in the children's form. In the early stage, the enchondral growth zone expands, loosens due to resorption bone tissue. In the future, the femoral head begins to slowly and gradually slide down, inwards and backwards, i.e., epiphysiolysis of the femoral head develops.
Symptomatic varus deformity is caused by a pathological process of the femoral neck or its upper metadiaphysis.

Valgus deformity of the proximal femur- deformity opposite to varus. It is congenital and acquired. If normally the cervical-diaphyseal angle ranges from 115-140°, then with valgus deformity it can approach 180°, then the axis of the femoral shaft serves as a direct continuation of the axis of the neck.

Congenital dislocation of the hip- population frequency 0.2-0.5%. It accounts for 3% of orthopedic diseases. The frequency of hip dysplasia is 16 cases per 1000 births. The dislocation is unilateral and bilateral in 20-25% of cases. The basis for the occurrence of dislocation is hip dysplasia, affecting all its components: the acetabulum (hypoplasia, flattening), the femoral head (hypoplasia, slowing down ossification), the neuromuscular apparatus (developmental anomalies).

At congenital subluxation of the acetabulum underdeveloped, the head occupies an eccentric position. Then a congenital dislocation develops. The main clinical signs are: a symptom of slipping - a symptom of Marx (a symptom of instability, a click), limitation of hip abduction, asymmetry of the gluteal folds, shortening of the lower limb, and with the beginning of the child's walking - gait disturbance.

Main radiological symptoms: in the absence of ossification nuclei, a vertical line passing through the upper outer protrusion of the acetabulum crosses the inner edge of the so-called femoral beak, which is more distant from the ischium than on the healthy side; the index of the acetabulum (acetabular index) reaches 35-40°; the ledge-like line of Menard - Shenton and the dashed line of Calvet are characteristic; the distance from the most protruding proximal surface of the thigh to the Hilgenreiner line (acetabular line connecting both Y-shaped cartilages) is less than 1 cm.

In the presence of nuclei ossification in addition to these symptoms, the following are revealed: the Hilgenreiner line crosses the head or is located below it; ossification on the side of the dislocation is delayed, the point of ossification of the head is smaller, the sciatic-pubic synchondrosis is open more widely, on the side of the dislocation there is atrophy of the bones, deformity of the head, shortening and thickening of the femoral neck, antetorsion of the neck. The horizontal line drawn along the lower edge of the femoral neck passes above the so-called teardrop, or Kohler's comma, the Maykova-Stroganova symptom is characteristic - the “crescent figure” is superimposed on the medial contour of the femoral neck, etc.

Abstract

In most instances, a toddler is seen with unilateral varus of the tibia, usually the deformity appearing slightly more distal than the knee joint. Radiographs of the focal fibrocartilaginous dysplasia show a characteristic abrupt varus at the metaphyseal - diaphyseal junction of the tibia. Cortical sclerosis is in and around the area of ​​the abrupt varus on the medial cortex. A radiolucency may appear just proximal to the area of ​​cortical sclerosis. The aetiology of such defects and the pathogenesis of the deformity are mostly unknown. Many of the associated factors suggest that the condition at least partly results from a mechanical overload of the medioproximal tibial physis.

The evaluation of a child with suspected pathologic tibia vara begins with a thorough history. A complete birth and developmental history should include the age at which the child began walking. The medical history should identify any renal disease, endocrinopathies, or known skeletal dysplasia. The physical examination should also include the child’s overall lower extremity alignment and symmetry, hip and knee motion, ligamentous hyperlaxity, and tibial torsion.

We describe on a 17-year-old-girl who manifests severe short stature associated with multiple orthopaedic abnormalities, namely, bilateral coxa vara and tibia vara. Radiographic documentation showed bilateral and symmetrical involvement of the lower limbs with the extensive form of fibrocartilaginous dysplasia, osteoporosis, and osteolytic lesions. The constellation of the malformation complex of osteolytic lesions, fibrocartilaginous changes and the polycystic like fibromas are not consistent to any previously published reports of fibrocartilaginous dysplasia. To the best of our knowledge, it seems that fibrocartilaginous changes are part of a novel type of skeletal dysplasia.


Introduction

The bone changes in our patient are somehow similar but not consistent and or diagnostic with polyostotic fibrous dysplasia (FD). A fibrocartilaginous dysplasia (FCD) commonly occurs in the lower extremities, especially in the proximal femur, leading to disabling deformity of the limb . In fibrocartilaginous dysplasia, the cartilage may develop in only one or in several segments of the affected bones. The appellation fibrocartilaginous dysplasia (FCD) has been used for those cases in which the cartilage is abundant. In the latter situation, extensive deformity of the bone may develop and lead to significant therapeutic problems. Radiologically, FCD has been described as a lucent lesion, with well-to-ill defined borders, usually containing scattered punctate to ring-like annular calcification. The calcification may be so extensive as to mimic an enchondroma or chondrosarcoma. Histologically, FCD differs from conventional FD only by its additional component of cartilage, with the benign-appearing spindle cell stroma and irregular shaped trabeculae of metaplastic woven bone found in both. The origin of the cartilage in FCD is controversial, some believing that it derives from offshoots or the rest of the epiphyseal plate that proliferate and grow . Others believe that it arises by direct stromal metaplasia, or that it develops from both processes. The rare occurrence of FCD in the calvarium and vertebral body , sites lacking an epiphyseal plate, would argue against the latter as the site of origin, at least in some cases. However, the irregularly bordered epiphyseal plates is some cases of FCD, with long columns of cartilage streaming into the adjacent metaphysis, would support this as a site origin for some of the cartilage . None, of the above mentioned clinical entities were compatible with our patient. Generalized osteoporosis associated with numerous osteolytic changes and bands of fibrocartilaginous dysplasia were the main abnormal characteristics observed in our patient.

clinical report

A-17-year-old-girl was referred to our department for clinical evaluation. She was a product of full term uneventful gestation. At birth, her growth parameters were around the 50th percentile. The mother was a 35-year-old gravida 2 abortus 0 married to a 43-year-old- unrelated man. She had no history of serious illnesses, apart from two femoral fractures were recorded at the age of 6 years. No more fractures were recorded thereafter. Her subsequent course of development was within normal limits. Since puberty the girl attained very short stature associated with bilateral tibia vara.

Clinical examination at the age of 17-years showed severe short stature of -3SD, her OFC was around the 50 percentile as well as her weight. No dysmorphic facial features were noted. Musculoskeletal examination showed mild ligamentous laxity of the upper limbs, though restrictions of the joints mobility were observed in her lower limbs. Her upper limbs were of normal development and her spine showed no peculiar deformities with normal trunk development. Her hands and feet were normal. Examination of the lower limbs showed very short lower segment in comparison with a normally developed upper segment. Muscular wasting was a notable feature. In her early life she was investigating for myopathy. Serum creatine kinase and plasma lactate were normal. electromyography showed minimal changes, and past muscle magnetic imaging (MRI) showed non-specific and non-diagnostic changes. Muscle biopsy and muscle respiratory chain were normal as well. No definite diagnosis has been established since the muscle biopsy and the other investigations were non-compatible with myopathy. Hormonal investigations included thyroid hormones; adrenocorticotropic hormone and growth hormone were negative as well.

Radiographic examination: AP radiograph of the pelvis showed bilateral coxa vara associated with expansile lytic lesion with ground glass matrix was seen bilaterally involving the proximal femora shaft and the greater trochanter with significant deformity seen in the proximal femoral region. Ring-like calcification suggesting cartilage was well appreciated. Note the hypoplastic capital femoral epiphyses and the defective modeling of the neck of the femur. There is a shortage of the femoral neck with pathologic ATD (articular trochanteric distance) of (minus) 7 mm left and (minus) 5 mm right (Fig. 1).

Lateral radiograph of the inferior femora and the super tibiae showed abundant calcification intermixed with areas of osteolytic lesions. Note multiple lucent lesions with bony islands and linear sclerotic changes, which extend from the epiphyses to involve the shafts (Fig. 2).

AP knees and lower femora radiographs showed a combination of osteoporosis, osteolytic islands along the cortices, and fibrocartilaginous changes (Fig. 3).

Lateral skull radiograph showed areas of osteolytic changes along the frontal and temporal bones, and osteolytic like area covering the most of the lambdoid sutures (Fig. 4).

AP radiograph of the thorax showed areas of multiple lucent lesions with bony islands and linear sclerotic changes along the Ribs (Fig. 5). Lateral spine radiograph showed normal vertebral anatomy with no trace of osteogenic lesions (Fig. 6).

Some of the bone lesions were tracer avid on Tc-99m MDP bone scans. Bone lesions showed non-specific increased 99m-Tc MDP. The bone scintigraphy role was helpful in conjunction with radiography to detect polyostotic involvement in different bones.

Discussion

Fibrocartilaginous dysplasia is a variant of fibrous dysplasia showing extensive cartilaginous differentiation (enchondroma-like areas). The amount of cartilage varies from case to case. This has been reported more commonly in polyostotic disease. It is well recognized that FD may contain cartilage, the amount of which, however, is variable. Lichtenstein and Jaffe in their original article on FD were of the opinion that cartilage was an integral part of the dysplastic process . Kyriakos et al. found 54 cases of FD in which cartilaginous differentiation was observed. At times this cartilage is abundant, such cases being designated under the rubric of either “fibrochondrodysplasia” a term introduced by Pelzmann et al. in 1980, or, more frequently as “fibrocartilaginous dysplasia” . Radiologically, FCD is similar to conventional FD with the addition, in most cases, of ring-like (annular) or scattered punctate to flocculent calcifications that may be so extensive as to simulate a primary cartilaginous lesion. In polyostotic FD, the occurrence of lucent columns of uncalcified cartilage may produce a streak-like radiologic pattern that mimics that of enchondromatosis (Ollier’s disease). The abundant cartilage has also occasionally led to a histologic misdiagnosis of chondrosarcoma arising in FD. FCD has no relationship to the abnormality termed focal fibrocartilaginous dysplasia that involves the pes anserinus and causes tibia vara in young children.

Histologically, FCD differs from conventional FD only by its additional component of cartilage, with benign appearing spindle cell stroma and irregularly shaped trabeculae of metaplastic woven bone found in both. The cartilage islands are well circumscribed, round nodules rimmed by a layer of woven or lamellar bone developing by enchondral ossification. At times the large cartilage islands may show increased cellularity, binucleate cells and nuclear atypical which could lead to a misdiagnosis of chondrosarcoma. The cartilaginous component can be massive as to mimic a chondroid neoplasm.

The key to the diagnosis is the identification of the classical areas of FD. Malignant transformation in FCD is a rare entity. Ozaki et al. reported a case of de-differentiated chondrosarcoma arising in a case of Albright’s syndrome, probably arising in a pre-existing FCD.

Idiopathic osteolysis, or “disappearing bone disease”, is an extremely rare condition characterized by the spontaneous onset of rapid destruction and resorption of a single bone or multiple bones. This results in severe deformities, with joint subluxation and instability. Hardegger et al. described the most commonly accepted classification; type 1, hereditary multicentric osteolysis with dominant transmission; type 2, hereditary multicentric osteolysis with recessive transmission, type 3, nonhereditary multicentric osteolysis with nephropathy; type 4, Gorham-Stout syndrome; and type 5, Winchester syndrome defined as a monocentric disease of autosomal recessive inheritance. Gorham disease has been considered as the most common form of idiopathic osteolysis. It may appear in any part of the skeleton and has been described in shoulder, pelvis, proximal femur, skull, and spine. It often involves multiple contiguous bones (ribs and spine, or pelvis, proximal femur, and sacrum). Presenting symptoms may be limb pain or weakness and depend on the site of involvement. The massive osteolysis results from vascular proliferation or angiomatosis within the involved bones and the surrounding soft tissue are characteristic features in connection with Gorham disease. Renal involvement is another clinical entity which is characterized by more severe and occurs more frequently in type 3 of Hardegger classification.

Conclusion

FD may show cartilaginous foci, the amount of which is variable with no bilateral or symmetrical presentation. As observed by many authors, the presence of cartilage is an indicator of future progressive bone deformity. The cartilaginous differentiation in FCD can be easily mistaken for a benign or malignant chondroid neoplasm. In this patient and because of logistical reasons we were unable to carry on histological examinations. Our findings however might signify a new variant of FCD with bilateral and symmetrical involvement of the lower limbs and of less degree of involvement of the thorax. Neither the spine nor the hands were involved in this pathological process. The overall clinical and radiographic phenotypes of our current patient were not consistent with any previously described conditions of fibrocartilaginous changes. There is another diagnostic possibility, which is, cystic angiomatosis. Of course, the possibility is less likely because of generalized osteopenia and short stature. We might postulate that this patient is another variant of Moog et al. but nevertheless, the wormain bones described by Moog et al. and the cortical lesions are to certain extent different. We confess that there were some limitations in this paper; firstly pre-pubertal images were not available; secondly, the histological examination was not performed because of logistical reasons and for the same reason next generation exome sequencing has not been organized.

Additional information

Funding. There is no source of funding.

Conflicts of interest. The authors declare no conflicts of interest.

ethical review. The legal guardians of the patient gave informed consent to process and publish personal data.

Acknowledgment. We wish to thank Mr. Hamza Al Kaissi student at the Slovak Medical University, Bratislava for his help in translating the German literature. We also wish to thank the patient’s family for their collaboration and permission to publish the clinical and the radiological data of their daughter.

Ali Al Kaissi

Ludwig Boltzmann Institute of Osteology, Hanusch Hospital, WGKK and AUVA Trauma Center Meidling, First Medical Department, Hanusch Hospital; Orthopedic Hospital of Speising, Pediatric Department

MD, MSc, Ludwig-Boltzmann Institute of Osteology at the Hanusch Hospital of WGKK and AUVA Trauma Center Meidling, First Medical Department and Orthopedic Hospital of Speising, Pediatric Department

Franz Grill

MD, Orthopedic Hospital of Speising, Pediatric Department

Rudolf Ganger

Orthopedic Hospital of Speising, Pediatric Department

MD, PhD, Orthopedic Hospital of Speising, Pediatric Department

Susanne Gerit Kircher

Medizinische Universität, Department für Medizinische Genetik

MD, MSc, Medizinische Universität, Department für Medizinische Genetik

  1. Muezzinoglu B, Oztop F. Fibrocartilaginous dysplasia: a variant of fibrous dysplasia. Malays J Pathol. 2001;23(1):35-39.
  2. World Health Organization classification of tumors, pathology and genetics of tumors of soft tissue and bone. Ed by C.D.M. Fletcher, K.K. Unni, F. Mertens. Lyon: IARC press; 2002.
  3. Harris WH, Dudley HR, Jr, Barry RJ. The natural history of fibrous dysplasia. An orthopaedic, pathological, and roentgenographic study. J Bone Joint Surg Am. 1962;44-A:207-233.
  4. Wagoner HA, Steinmetz R, Bethin KE, et al. GNAS mutation detection is related to disease severity in girls with McCune-Albright syndrome and precocious puberty. Pediatric Endocrinol Rev. 2007;4 Suppl 4: 395-400.
  5. Vargas-Gonzalez R, Sanchez-Sosa S. Fibrocartilaginous dysplasia (Fibrous dysplasia with extensive cartilaginous differentiation). Pathol Oncol Res. 2006;12(2):111-114. doi:10.1007/bf02893455 .
  6. Lichtenstein L, Jaffe HL. Fibrous dysplasia of bone. A condition affecting one, several or many bones, the graver cases of which may present abnormal pigmentation of skin, premature sexual development, hyperthyroidism or still other extraskeletal abnormalities. Arch Pathol. 1942;33:777-816.
  7. Forest M, Tomeno B, Vanel D. Orthopedic surgical pathology: diagnosis of tumors and pseudotumoral lesions of bone and joints. Edinburgh: Churchill Livingstone; 1998.
  8. Morioka H, ​​Kamata Y, Nishimoto K, et al. Fibrous Dysplasia with Massive Cartilaginous Differentiation (Fibrocartilaginous Dysplasia) in the Proximal Femur: A Case Report and Review of the Literature. Case Rep Oncol. 2016;9(1):126-133. doi:10.1159/000443476 .
  9. Hermann G, Klein M, Abdelwahab IF, Kenan S. Fibrocartilaginous dysplasia. Skeletal Radiol. 1996;25(5):509-511. doi:10.1007/s002560050126 .
  10. Ishida T, Dorfman HD. Massive chondroid differentiation in fibrous dysplasia of bone (fibrocartilaginous dysplasia). Am J Surg Pathol. 1993;17(9):924-930.
  11. Kyriakos M, McDonald DJ, Sundaram M. Fibrous dysplasia with cartilaginous differentiation (“fibrocartilaginous dysplasia”): a review, with an illustrative case followed for 18 years. Skeletal Radiol. 2004;33(1):51-62. doi: 10.1007/s00256-003-0718-x .
  12. Pelzmann KS, Nagel DZ, Salyer WR. Case report 114. Skeletal Radiol. 1980;5(2):116-118. doi:10.1007/bf00347333 .
  13. Bhaduri A, Deshpande R.B. Fibrocartilagenous mesenchymoma versus fibrocartilagenous dysplasia: are these a single entity? Am J Surg Pathol. 1995;19(12):1447-1448.
  14. Ozaki T, Lindner N, Blasius S. Dedifferentiated chondrosarcoma in Albright syndrome. A case report and review of the literature. J Bone Joint Surg Am. 1997;79(10):1545-1551.
  15. Hardegger F, Simpson LA, Segmueller G. The syndrome of idiopathic osteolysis. classification, review, and case report. J Bone Joint Surg Br. 1985;67-B(1):88-93. doi: 10.1302/0301-620x.67b1.3968152 .
  16. Al Kaissi A, Scholl-Buergi S, Biedermann R, et al. The diagnosis and management of patients with idiopathic osteolysis. Pediatric Rheumatol. 2011;9(1):31. doi: 10.1186/1546-0096-9-31 .
  17. Moog U, Maroteaux P, Schrander-Stumpel CT, et al. Two sibs with an unusual pattern of skeletal malformations resembling osteogenesis imperfecta: a new type of skeletal dysplasia? J Med Genet. 1999;36(11):856-858. doi: 10.1136/jmg.36.11.856 .

Supplementary files

Supplementary Files action
1. Fig. 1. AP radiograph of the pelvis showed bilateral coxa vara associated with expansile lytic lesion with ground glass matrix was seen bilaterally involving the proximal femora shaft and the greater trochanter with significant deformity seen in the proximal femoral region. Ring-like calcification suggesting cartilage was well appreciated. Note the hypoplastic capital femoral epiphyses and the defective modeling of the neck of the femur. There is a shortage of the femoral neck with pathologic ATD (articular trochanteric distance) of (minus) 7 mm left and (minus) 5 mm right (93KB)
2. Fig. 2. Lateral radiograph of the inferior femora and the super tibiae showed abundant calcification intermixed with areas of osteolytic lesions. Note multiple lucent lesions with bony islands and linear sclerotic changes, which extend from the epiphyses to involve the shafts (102KB)
3. Fig. 3. AP knees and lower femora radiographs showed a combination of osteoporosis, osteolytic islands along the cortices, and fibrocartilaginous changes (111KB)
4. Fig. 4. Lateral skull radiograph showed areas of osteolytic changes along the frontal and temporal bones, and osteolytic like area covering the most of the lambdoid sutures (90KB)
5. Fig. 5. AP radiograph of the thorax showed areas of multiple lucent lesions with bony islands and linear sclerotic changes along the Ribs (92KB)
6. Fig. 6. Lateral spine radiograph showed normal vertebral anatomy with no trace of osteogenic lesions. (63KB)

One of the rare anomalies in the development of the femur is their deformity of the varus type. The disease occurs no more often than in 0.3-0.8% of cases among newborns. Along with valgus curvature of the proximal end of the femur, congenital varus deformity of the femur is a skeletal defect. It can lead to serious violations of the functioning of the musculoskeletal system.

Description of varus deformity of the hips

The basis of the curvature of the hip joints according to the varus type is the shortening of the neck of the femur and a decrease in the degree of the neck-diaphyseal angle. Another name for the disease is juvenile epiphysiolysis, although in fact the latter is one of the forms of hip deformity and is very rare, only in adolescence. Changes in the hip joints in this pathology are significant - dystrophy of the spongy tissue of the neck, bone destruction, formation of cysts, fibrosis phenomena.

Varus-type hip deformity includes a whole range of symptoms from the side lower extremities. With this disease, the following symptoms can be combined:

  • change in the shape of the articular heads of the pelvic bones;
  • leg shortening;
  • contractures of the hip joint;
  • dysplasia, dystopia of leg muscles;
  • lumbar lordosis.

In a child with hip deformity, a serious violation of rotation and abduction of the leg is noted, so the gait becomes “duck”. When an anomaly occurs in a newborn, then the leg is already shorter than the second one from birth, and the trochanter of the thigh is located higher than expected. If the pathology is not treated for a long time, it continues to progress, ossification occurs. The femoral neck is bent, the diaphysis is shortened.

When a varus-type joint deformity occurs at the age of 3-5 years, a trihedral bone fragment appears in the femoral neck. Visually, the head and neck of the femur resemble an inverted letter U. The joint space becomes tortuous, the edges of the bone are jagged, uneven, and foci of sclerosis appear in them. After the gap of the hip joint expands to 1-1.2 cm, the neck is shortened, and the head ceases to develop normally.

If in the childhood form of varus curvature there are changes in the bone zone, then in the youthful form there are violations in the growth zone. The latter is loosened, the bone is resorbed, the head slowly slides down. Therefore, the pathology is called "epiphyseolysis of the femoral head."

Causes of the disease

Usually, congenital varus deformity becomes a consequence of intrauterine damage to the cartilage of the femur or a violation of the process of their compaction. In 2/3 of the patients the defect is unilateral, in other cases it is bilateral. Thus, the disease occurs due to various problems in the embryonic period, which can happen for such reasons:

  • severe maternal infections during pregnancy;
  • alcohol abuse, drug use, toxic drugs;
  • poisoning, intoxication;
  • advanced age of the mother;
  • endocrine diseases;
  • the influence of radiation.

As for the acquired forms, they can occur for various reasons. So, juvenile epiphyseolysis develops at 11-16 years old - during puberty, or precedes puberty. The head of the femur begins to deform precisely against the background of a general restructuring of the body, when some parts of the skeleton are most vulnerable. It is believed that hormonal disorders become the cause of pathology in adolescents, therefore other phenomena are also often observed in patients:

  • lack of secondary sexual characteristics;
  • delay in menstruation in girls;
  • too tall;
  • obesity.

Also, varus deformity of the femur is associated with trauma and rickets, with a number of systemic diseases - pathological bone fragility, fibrous osteodysplasia, dyschondroplasia. Also, the cause of the pathology can be:

  • failed hip surgery
  • osteomyelitis;
  • bone tuberculosis;
  • osteochondropathy.

Symptoms of the disease

The children's form of pathology usually begins to develop no later than 3-5 years, since during this period there is an increase in the load on the lower limbs. Parents may experience the following symptoms:

  • lameness after a long walk;
  • pain in the legs in the afternoon due to fatigue;
  • inability to run for a long time, play outdoor games;
  • discomfort in the thigh and knee, in the popliteal region;
  • pain in the knee joint.

Over time, the leg on the affected side becomes somewhat thinner, hip abduction becomes more difficult, and more so on the inside (on the contrary, it can increase on the outside). In a number of children, the symptomatology begins with pain in the knee, and it is not always possible to establish a connection with a hip lesion immediately.

Juvenile forms of hip deformity often do not give clinical signs at all, only in advanced cases they begin to manifest themselves. There is a slight lameness, increased fatigue when walking. Some adolescents have a protruding stomach, there is a pathological lordosis of the spine. The strength and tone of the gluteal muscles are reduced. With bilateral damage to the hips, the child begins to walk like a duck, waddling, swaying.

Classification of pathology

Due to the appearance and radiological signs, the deformity of the femur can exist in the following forms: children's, youthful, symptomatic, rickets, tuberculosis. Also, the disease is isolated or is reflected in other joints, feet of the child. Another classification involves the division of the disease into three stages (degrees).

First degree of severity

At the first stage, pathological changes begin in the growth region of the femur. Gradually, its loosening and expansion occurs, but the epiphysis does not move.

Second degree of severity

At the second stage, progression of the processes of bone tissue restructuring and displacement of the epiphysis is observed. The picture shows a thinning of the femoral neck, the fuzziness of its structure.

Third degree of severity

At the third stage, a complication of the pathology is already registered - deforming arthrosis. There is also atrophy of the muscles of the lower limb and marked changes in gait.

Diagnosis of varus deformity

The most popular and informative method of diagnosis is radiography of the hip joint. At the very beginning of the hip deformity, heterogeneity of the bone mass in the region of the femoral neck is revealed. Later, other structural changes appear, as well as violations of the anatomy of the hip joint.

When examined by an orthopedist, violations in adduction and abduction of the limb on one or both sides are revealed. In parallel, kyphosis, scoliosis, lordosis, wedge-shaped deformity of the vertebrae, and other disorders in the knees, sacrum, and ankles can be diagnosed.

Treatment of pathology

In the early stages, conservative therapy helps well, later it is used surgical treatment. Initially, as a rule, the patient is hospitalized for limb traction (skeletal traction), after which treatment is continued at home.

Conservative treatment

With a congenital form of pathology, conservative therapy is indicated for all babies up to 3 months of age. The goals are to normalize the blood supply to the hip joint and accelerate bone recovery, improve the tone of muscle tissue, and reduce the effect of muscles on the state of the joint. For this, the following therapies are performed:

  • wide swaddling for 14 days, after - Freyka pillow for 2.5 months;
  • sollux, paraffin applications;
  • from 6-8 weeks - electrophoresis on the joint area with calcium, phosphorus, with vasodilators - on the area of ​​the sacral spine.

Other forms of varus deformity are treated with the complete exclusion of any load on the leg, strict bed rest. The patient is given a plaster cast of the limb, traction with a load of up to 2 kg. Treatment can take several months, so it is often carried out in specialized sanatoriums.

Operation

If the processes of bone remodeling have already ended and there is a pronounced degree of varus-type hip deformity, surgical treatment should be planned. It will help lengthen the limb, restore the integrity of the articular surfaces and prevent the development of coxarthrosis.

In babies older than 3 months, with contractures of the hip joint, surgery is also indicated. The goals are to create conditions for the correct development of the head of the bone and to prevent deformation of the cervical-diaphyseal angle.

During the operation, the adductor muscles of the thigh, the wide fascia of the thigh, and a number of tendons are dissected. Fibrous cords are removed in the area of ​​the gluteal muscle. In children from 3 years of age, an additional corrective osteotomy is performed if there is excessive ossification of the femoral neck. The operation includes a neck plastic surgery. It is performed in the second stage after the healing of the bone tissue - a few months after the first intervention.

Rehabilitation treatment

After the operation, the patient is required to be prescribed a complex of exercise therapy, physiotherapy, drug general strengthening treatment. Children use orthoses and other orthopedic devices. So, with a curvature of the hip in adolescents, the use of orthoses can continue for several years. Dispensary observation is carried out until the child reaches the age of 18 years.

If left untreated, the pathology will steadily progress, which causes the formation of a false joint of the femoral neck (in 50-70% of cases). Further, coxarthrosis develops, which, ultimately, will require joint arthroplasty. With early treatment, the outcome is often favorable.

As well as the occurrence of hip deformities in general, it is based on various reasons. Part of the deformities comes from changes in the hip joint and femoral neck. Deformities in the area of ​​the metaphysis and diaphysis of the thigh can be congenital, rachitic, inflammatory, can be associated with trauma and various tumors.

Symptoms of deformity of the femoral neck.

Deformation of the femoral neck often develops in early childhood, is often the result of rickets, may depend on congenital and dysplastic changes in the skeletal system, and is less often associated with trauma.

The curvature of the femoral neck is characterized by a decrease in the angle between the diaphysis and the femoral neck (to a straight or even sharp one) and is called coxa vara. On the basis of anatomical changes, functional disorders occur, manifested by rocking of the body when walking, limitation of hip abduction, lameness as a result of shortening of the leg.

Swinging of the body when walking at the moment of loading on the sore leg depends on the functional insufficiency of the middle and small gluteal muscles due to the displacement of the thigh upwards. To keep the pelvis in a horizontal position, the patient is forced to tilt the body towards the affected leg. Thus, the so-called duck gait is formed. Often there are complaints of increasing weakness of the lower limb, fatigue, pain when walking and standing.

Deformation related to the previous one are X-shaped legs. The development of this deformity is associated with an uneven load on the femoral condyles and their uneven growth: the growth of the internal condyle gradually leads to the formation of a valgus curvature of the knee joint. Clinically, this deformity is manifested by the fact that the thigh and lower leg form an angle in the knee joint that is open to the outside.

In a child with a similar deformity, the knee joints are in close contact, while the feet are at a great distance from one another. In an effort to bring the feet together, the knee joints come one after the other. Such a deformity of the knee joints is often accompanied by a valgus installation of the feet (deflection of the calcaneal bones outwards). This deformity can lead to pain due to the progressive development of flat feet.

At the heart of another deformity of the legs and knee joints, the O-shaped curvature of the legs, most often lies rickets. An arcuate curvature of the bones of the lower leg with a bulge outward develops in the process of vertical load under the influence of muscle traction during softening of the bones by a rachitic process. The curvature of the lower leg is enhanced under the influence of the traction of the triceps muscle of the lower leg, acting in the direction of the chord forming the arc.

The vicious position of the bones is fixed in the process of their asymmetric growth. The disease is manifested by a duck gait, a positive Trendelenburg symptom, limited abduction and rotation in the hip joint, however, unlike congenital hip dislocation, the head of its valgus deformity is palpable in the Scarpov triangle.

Causes of deformity of the femoral neck.

The causes of valgus deformity of the femoral neck are varied. Allocate congenital, children's or dystrophic, youthful, traumatic and rachitic deformities. In addition, valgus curvature of the femoral neck is observed in systemic diseases: fibrous osteodysplasia, pathological bone fragility, dyschondroplasia. Deformity may be the result of surgical interventions in the femoral neck or any pathological conditions of the bone in this area (consequences of osteomyelitis, tuberculosis, subcapital osteochondropathy).

Congenital valgus deformity of the femoral neck is more often bilateral, and then the disease is detected with the beginning of the child's walking in a characteristic duck gait, which often suggests a congenital dislocation of the hip. In addition, on examination, there is a limitation in the spread of the legs and a high standing of the large skewers. X-ray examination makes it possible to diagnose the disease. Often, the deformity of the femoral neck is combined with other congenital defects: shortening of the limb, a violation of the shape of other joints.

Children's viral deformity of the femoral neck is more often unilateral and is associated with dystrophic processes as a result of trophic disorders and is accompanied by bone tissue restructuring in the form of aseptic necrosis. The disease begins at the age of 3-5 years, under the influence of the load, the deformity of the femoral neck progresses. Clinically, the disease is manifested by lameness, pain, especially after a long walk, run. The affected limb may be shorter and thinner, and hip abduction is limited. The greater trochanter is located above the Roser-Nelaton line, a positive Trendelenburg sign is noted.

In other words clinical manifestations in many ways identical to congenital dislocation of the hip. However, there will be no symptoms characteristic of dislocation, such as displacement of the thigh along the longitudinal axis (Dupuytren's symptom), a symptom of a non-disappearing pulse with pressure on the femoral artery in the Scarp triangle.

Diagnosis of deformity of the femoral neck.

Diagnosis in the vast majority of cases does not cause any difficulties for a traumatologist or any other specialist. In order to clarify the position of the end of the femur and exclude probable bone damage, it is necessary to conduct an x-ray examination. Moreover, it must be in two projections.

In the same case, if the diagnosis is in doubt, an MRI of the entire described joint is performed.

Treatment of deformity of the femoral neck.

Correction of such a deformity is effective at the beginning of their formation (on the 1st-2nd year of life). The principle of complex therapy common to most orthopedic deformities is also valid for this group of deformities of the lower extremities. Application and combined with orthopedic treatment (appointment of special splints, wearing special devices).

Treatment is operative.

It is carried out in two directions: therapy of the causes of deformity and surgical (the deformity itself). Based on cases of detection of the disease, it is noted that valgus deformity of the femoral neck appears in a patient from birth. There are rare cases when the deformity occurs with a traumatic or paralytic etiology.

Before starting the operation, it is required to plan the upcoming operation. Find out what methods and constructions can be applied in this case. Thus, the surgeon faces the following questions:

  • Simultaneous or staged elimination of hip deformity.
  • Limb length adjustment.
  • Removal of old processes in the event that operations of this type were carried out.
  • Design and installation of the endoprosthesis.

There are more than 100 methods of treating valgus deformity of the femoral neck:

  • Exostectomy (removal of part of the head of the bone);
  • Restoration of ligaments;
  • Replacement with an implant;

In the case when the femoral neck is replaced with an implant, local or general anesthesia is performed before the operation. The surgeon then makes a small incision. Next, the surgeon removes the femoral neck and installs an endoprosthesis that ideally repeats its shape. The prosthesis facilitates movement, helps to correct gait, improve the quality of life, get rid of pain. There are many types of prostheses, which are selected according to the specific case of the disease.

Prevention of deformity of the femoral neck.

In order to prevent dislocation in the hip area, it is recommended to carefully monitor the safety in Everyday life and during sports activities.

This raises the need for:

  • training of various muscle groups, rational physical activity;
  • the use of exceptionally comfortable clothing and footwear to prevent falls;
  • the use of professional protective equipment throughout sports activities. We are talking, at a minimum, about knee pads and hip braces;
  • avoiding any trips in ice, paying attention to slippery and wet surfaces.

In order to fully restore the hip joint after dislocation, it will take, if there are no complications, from 2 to 3 months. This period can only be lengthened if there are concomitant fractures. So, the doctor may insist that a non-long-term skeletal type traction be carried out with further sets of exercises. This is done with the help of a device of continuous inactive movement.

Independent movement using crutches is possible only in the absence of any pain. Until the moment when lameness disappears, it is recommended to resort to additional aids for moving, for example, a cane.

After that, it is recommended to use general strengthening drugs that will affect the structure of bone tissue. It is also important to carry out certain exercises, the list of which should be compiled by a specialist. The regularity of their implementation will be the key to recovery. In addition, it is necessary to treat the damaged area of ​​the thigh as carefully as possible, because now it is one of the weakest points in the body.

Keeping in mind all the rules of prevention and treatment, it is more than possible to quickly and permanently get rid of any consequences of hip dislocation while maintaining the optimal rhythm and tone of life.

Varus deformity of the femoral neck Cervical-diaphyseal angle less than average (120 -130°) Causes: § Congenital dislocation of the hip § Juvenile epiphysiolysis § traumatic § rachitic deformity § in case of systemic diseases: fibrous osteodysplasia, pathological bone fragility, dyschondroplasia § consequence of surgical interventions in the area femoral neck § consequences of osteomyelitis, tuberculosis, subcapital osteochondropathy

Clinic: With congenital duck gait, rapid fatigue in the hip joint during walking. functional shortening of the limb by 3-5 cm or more; limitation of abduction in the hip joint; positive Trendelenburg symptom. Treatment: Subtrochanteric osteotomy

Valgus deformity of the femoral neck Increase in the neck-diaphyseal angle. ü Congenital ü Traumatic ü Paralytic Clinic: no visible deformities § With concomitant deformities of the knee and foot, gait changes, cosmetic defects Treatment: 1) exercises and corrective postures (“in Turkish”) 2) operative: subtrochanteric osteotomy of the femur.

Varus and valgus deformity of the knee joints Causes: § congenital, § rickets, § early rising to the feet Varus deformity - the angle is open inwards, Onogi

Valgus deformity Varus deformity increase in the external condyle, decrease in the internal - compression of the internal meniscus increase in the internal condyle, decrease in the external - compression of the external meniscus the joint space is wider on the outside the joint space is wider on the inside the ligaments are stretched, strengthening the knee joint from the later. the sides are stretched ligaments that strengthen the knee joint on the medial side of the lower leg are often curved with a bulge outward, flat-varus foot setting (clubfoot) flat-valgus foot setting (flat feet) in severe cases: rotation (turn) of the thigh outward, and the lower leg (its lower third) inwards. v Unilateral v Bilateral: symmetrical (concordant deformity) / discordant deformity.

Diagnosis 1) Goniometer 2) Distance m/d medial. ankles (exceeds 1.5-2.0 cm - up to 2 years, 3 cm - 3-4 years and 4 cm - older) 3) X-ray - 3 degrees

Treatment 1) 2) 3) 4) Massage Therapeutic gymnastics Orthopedic shoes Surgical treatment - valgus and varus osteotomy

Flat feet - a change in the shape of the foot, characterized by the omission of its longitudinal and transverse arches. TYPES: longitudinal flatfoot transverse flatfoot longitudinal-transverse

Foot arches Longitudinal arches: 1) External / cargo (calcaneal, cuboid, IV and V metatarsal bones) 2) Internal / spring (talar, scaphoid and I, III metatarsal bones) Transverse arch (metatarsal bones heads)

Etiology Acquired Rachitic platypodia Paralytic platypodia (AFTER POLIO) Traumatic platypodia (ANKLE, CANEAL, AND TARSAL FRACTURES) Static platypodia (excessive load on the foot) Congenital

Clinic Complaints: § fatigue, pain in the calf muscles by the end of the day § pain in the arch of the foot when standing and walking Typical signs: Ø lengthening of the foot and expansion of its middle section Ø decrease or complete disappearance of the longitudinal arch (the foot rests on its entire plantar surface) Ø abduction (valgus abduction) of the forefoot (toe looks outward) Ø pronation (outward deviation) of the calcaneus over 5 -6 °; In this case, the inner ankle protrudes, and the outer one is smoothed.

Stages of flat feet q. Hidden stage q. Stage of intermittent flat feet q. Stage of development of a flat foot q. Stage of flat-valgus foot q. Contracture flatfoot

Diagnosis 2) Podometry according to Friedland - determination of the percentage ratio of the height of the foot and its length (N = 31 -29) 3) Line of Face - a line drawn from the top of the inner ankle to the lower surface of the base of the head of the I metatarsal bone (in N- does not cross the top of the navicular bone )

Diagnosis 4) Clinical method (normal vault 55-60 mm, angle 90◦) 5) X-ray method (normal vault 120-130◦, normal vault 35 mm)

Flatfoot degree I degree: Friedland index 25 - 27 clinical angle 105◦ radiological angle up to 140◦ arch height less than 35 mm II degree: radiological angle up to 150◦ arch height less than 25 mm signs of def. Osteoarthritis III degree: radiographic angle up to 170 -175 ◦ arch height less than 17 mm flatness of the forefoot

Treatment q In the stage of development of a flat foot: I degree: warm foot baths, massage, exercise therapy to strengthen the muscles of the lower leg, wearing arch support insoles II degree: + wearing orthopedic shoes III degree: + surgical treatment

q In the stage of contracture flat feet Non-operative: blockade of the posterior tibial nerve; ü plaster bandages Operative: ü three-articular arthrodesis of the foot (talonavicular, calcaneocuboid, subtalar) After the onset of arthrodesis, it is necessary to wear orthopedic shoes to form the arch of the foot

ü Operation according to F. R. Bogdanov - resection of the calcaneocuboid and talo-navicular joints with subsequent arthrodesis of these joints in the corrected position of the arches - lengthening of the tendon of the short peroneal muscle - transplantation of the tendon of the long peroneal muscle on the inner surface of the foot - lengthening of the calcaneal tendon with the elimination of pronation heel and abduction of the forefoot ü Kuslik M. I. operation - crescent-transverse resection of the foot - lengthening of the calcaneal tendon - transplantation of the tendon of the long peroneal muscle on the inner surface of the foot

Transverse flatfoot deformity of the foot, manifested by flattening of the distal metatarsus in combination with valgus deviation of the first finger, the development of deforming arthrosis of the first metatarsophalangeal joint and limitation of movement in this joint, as well as the occurrence of hammer-shaped deformity of the II-V fingers Causes: weakness of the ligamentous apparatus congenital / hormonal changes § ill-fitting shoes.

Treatment of transverse flatfoot Operations on the tendons of the muscles of the 1st finger (mm. extensor et flexor hallucis longus, t. Adductor ü transposition of the tendon of the long flexor of the 1st finger to the tendon of the long extensor ü Adductorothenotomy Operation of Schede-Brandes - resection of osteochondral exostosis of the head of the 1st metatarsal bone, resection base of the main phalanx of the 1st finger McBride's operation - cutting off the tendon of the adductor of the 1st finger from the base of the main phalanx and suturing it to the head of the 1st metatarsal bone

Hammer-shaped deformity of the fingers Ø with transverse flat feet Ø with children's cerebral palsy Ø poliomyelitis (with flat-valgus foot) Ø myelodysplastic hollow foot

Exostoses of the heads of the I and V metatarsal bones Subluxation valgus deviation