JBJS | The Prognostic Importance of the Ossific Nucleus in the Treatment of Congenital Dysplasia of the Hip*

The Journal of Bone & Joint Surgery, Volume 80, Issue 12

Articles | December 01, 1998

The Prognostic Importance of the Ossific Nucleus in the Treatment of Congenital Dysplasia of the Hip*

SCOTT J. LUHMANN, M.D.†; PERRY L. SCHOENECKER, M.D.†; ANN M. ANDERSON, R.N.†; GEORGE S. BASSETT, M.D.‡, ST. LOUIS, MISSOURI

View Disclosures and Other Information

Investigation performed at the Shriners Hospital for Children, St. Louis Unit, and the Department of Orthopaedic Surgery, St. Louis Children's Hospital, St. Louis

The Journal of Bone & Joint Surgery. 1998; 80:1719-27

5 Recommendations (Recommend) | 3 Comments | Saved by 3 Users Save Case

text A A A

Abstract

Ischemic necrosis of the femoral head occurring after the treatment of congenital dysplasia of the hip can negatively affect the long-term prognosis of the involved hip. Some investigators have suggested that the presence of the ossific nucleus of the femoral head at the time of closed or open reduction is associated with a lower rate of ischemic necrosis. This finding, if verified, could lead to a delay in the treatment of a dislocated hip until ossification of the femoral head has begun, which may be well after the age when the patient has started to walk.We conducted a computerized search of the medical records at our two tertiary-care children's hospitals to identify all patients with congenital dysplasia of the hip who had had a closed or open reduction between January 1, 1979, and December 31, 1993. One hundred and twenty-four patients (153 hips) who satisfied the criteria for inclusion were identified. The ossific nucleus was present in ninety hips and absent in sixty-three. Closed reduction was used in 112 hips and open reduction, in forty-one. Ischemic necrosis was identified in five hips (3 percent): four (6 percent) of the sixty-three hips that did not have an ossific nucleus and one (1 percent) of the ninety hips that had an ossific nucleus at the time of the reduction. With the numbers available for study, we could not detect a difference between these two groups. The age at reduction (p > 0.99), the method of reduction (p = 0.611), previous treatment with a Pavlik harness (p = 0.592), the use of preliminary traction (p = 0.602), concomitant procedures (p > 0.99), and a failure of the primary closed reduction (p = 0.579) were not associated with the development of ischemic necrosis after reduction.In our analysis of patients who were managed over a fifteen-year period, the data did not support the hypothesis that the presence of an ossific nucleus at the time of reduction of a congenitally dislocated hip is associated with a lower prevalence of ischemic necrosis of the femoral head. Sound operative principles dictate that operative reduction of a congenitally displaced hip should be performed when the child can be safely placed under anesthesia and without regard to the presence or absence of the ossific nucleus.

Figures in this Article

Introduction

Introduction | Materials and Methods | Results | Discussion | References

Most patients with congenital dysplasia of the hip who are first seen in the neonatal period can be definitively managed with a Pavlik harness. Early detection is optimum as it makes it possible to take advantage of the hip joint's remarkable capacity to remodel and makes it possible to use a Pavlik harness, which is associated with low morbidity^19,35,38,47. However, when a patient is first seen after the age of six months, which is generally thought to be too old for management with a Pavlik harness, or when management with a Pavlik harness has failed, it is necessary to perform a closed or open reduction of the dislocated hip followed by immobilization in a spica cast.

Complications from the treatment of congenital dysplasia of the hip are well documented and include ischemic necrosis of the femoral head, infection, osteochondritis dissecans, chondrolysis, trochanteric overgrowth, acetabular dysplasia, limb-length discrepancy, subluxation or dislocation of the hip, coxa valga or coxa vara, coxa magna, and deformity of the femoral head with incongruity of the joint and secondary osteoarthrosis^{8,12,15,25,39}. Of these, ischemic necrosis is one of the most devastating iatrogenic complications in the treatment of congenital dysplasia of the hip^{5,8,12,17,25,40}. The management of a child who has ischemic necrosis can be extremely difficult and may not improve the prognosis when there is severe involvement^12,39,47. Asphericity and irregularity of the femoral head, subluxation of the hip, and residual acetabular dysplasia after ischemic necrosis are indicators of a hip that is at risk for the development of early osteoarthrosis⁸. The importance of this sequela has been demonstrated in long-term studies of congenital dislocation of the hip in which a satisfactory late result was achieved in only 20 percent (six of thirty) to 41 percent (thirteen of thirty-two) of the hips that had ischemic necrosis after reduction^8,12,21,47. Therefore, prevention of ischemic necrosis is a primary consideration during the treatment of congenital dysplasia of the hip.

Since Salter et al.⁴⁰, in 1969, implicated the position of the hip during immobilization in a cast as a cause of necrosis, multiple factors have been reported to be important in the development of ischemic necrosis after reduction^{13,15,18,20,24,25,27,40,41}. In 1978, Fisher and Cary¹² proposed that children who did not have ossification of the femoral head at the time of reduction of a congenitally dislocated hip were at a higher risk for ischemic necrosis. In 1996, Segal et al.⁴⁴ identified a strong association between the absence of an ossific nucleus and an increased prevalence of ischemic necrosis. In their series, ischemic necrosis developed in seventeen (53 per cent) of thirty-two hips in which the ossific nucleus was absent at the time of reduction. Of twenty-five hips in which the ossific nucleus was present at the time of reduction, only one (4 percent) had changes of ischemic necrosis. These observations led to the hypothesis that the presence of the ossific nucleus at the time of reduction has a protective effect against the development of ischemic necrosis of the femoral head.

The purpose of the present study was to determine if the presence of the ossific nucleus at the time of reduction of a congenitally dislocated hip was associated with a lower prevalence of ischemic necrosis in our series of patients. Our null hypothesis was that the prevalence of ischemic necrosis is the same for patients who have an intact femoral ossific nucleus and for those who do not at the time of reduction of a congenitally dislocated hip.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Shriners Hospital for Children, St. Louis Unit, 2001 South Lindbergh Boulevard, St. Louis, Missouri 63131.

‡Department of Orthopaedic Surgery, St. Louis Children's Hospital, One Children's Place, St. Louis, Missouri 63110.

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

†Shriners Hospital for Children, St. Louis Unit, 2001 South Lindbergh Boulevard, St. Louis, Missouri 63131.

‡Department of Orthopaedic Surgery, St. Louis Children's Hospital, One Children's Place, St. Louis, Missouri 63110.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 1 Anteroposterior radiograph of the pelvis, made before reduction, in a seven-month-old child who had a dislocated right hip.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 2 Anteroposterior radiograph of the pelvis, made four years and eleven months after closed reduction of the right hip, demonstrating Bucholz and Ogden⁴ type-III involvement.

View Larger

TABLE I PREVALENCE AND CLASSIFICATION OF ISCHEMIC NECROSIS

*The values are given as the number of hips.

	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				No Evidence of Necrosis	Total
I	II	III	IV
Ossific nucleus*
Absent	1	0	4	0	58	63
Present	3	0	1	0	86	90
Total	4	0	5	0	144	153

Add to My JBJS

TABLE I PREVALENCE AND CLASSIFICATION OF ISCHEMIC NECROSIS

*The values are given as the number of hips.

	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				No Evidence of Necrosis	Total
I	II	III	IV
Ossific nucleus*
Absent	1	0	4	0	58	63
Present	3	0	1	0	86	90
Total	4	0	5	0	144	153

View Larger

TABLE II STATISTICAL ANALYSIS OF MEASURED VARIABLES WITH RESPECT TO THE PREVALENCE OF ISCHEMIC NECROSIS

*None of the findings were significant. †The ischemic necrosis was classified according to the system of Bucholz and Ogden⁴.

Factor	Types I through IV Ischemic Necrosis*†	Types II, III, and IV Ischemic Necrosis*†
Presence of ossific nucleus	p = 0.489	p = 0.160
Age at reduction
<6 mos.	p > 0.99	p > 0.99
<12 mos.	p = 0.732	p > 0.99
Unilateral compared with bilateral involvement	p > 0.99	p > 0.99
Treatment with Pavlik harness	p > 0.99	p = 0.592
Preliminary traction	p = 0.694	p = 0.602
Closed compared with open reduction	p = 0.059	p = 0.611
Adductor tenotomy	p = 0.494	p = 0.162
Varus rotational osteotomy	p = 0.685	p > 0.99
Failure of closed reduction	p = 0.150	p = 0.579
Failure of open reduction	p > 0.99	p > 0.99

Add to My JBJS

TABLE II STATISTICAL ANALYSIS OF MEASURED VARIABLES WITH RESPECT TO THE PREVALENCE OF ISCHEMIC NECROSIS

*None of the findings were significant. †The ischemic necrosis was classified according to the system of Bucholz and Ogden⁴.

Factor	Types I through IV Ischemic Necrosis*†	Types II, III, and IV Ischemic Necrosis*†
Presence of ossific nucleus	p = 0.489	p = 0.160
Age at reduction
<6 mos.	p > 0.99	p > 0.99
<12 mos.	p = 0.732	p > 0.99
Unilateral compared with bilateral involvement	p > 0.99	p > 0.99
Treatment with Pavlik harness	p > 0.99	p = 0.592
Preliminary traction	p = 0.694	p = 0.602
Closed compared with open reduction	p = 0.059	p = 0.611
Adductor tenotomy	p = 0.494	p = 0.162
Varus rotational osteotomy	p = 0.685	p > 0.99
Failure of closed reduction	p = 0.150	p = 0.579
Failure of open reduction	p > 0.99	p > 0.99

View Larger

TABLE III PREVALENCE OF ISCHEMIC NECROSIS BY TYPE OF REDUCTION

*With the numbers available, no significant relationship could be detected between the presence or absence of the ossific nucleus and the development of ischemic necrosis in the hips that had a closed (p = 0.312) or an open reduction (p > 0.99) reduction.

	No. of Hips	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				Total
I	II	III	IV
Open reduction*	41
Ossific nucleus absent	15	0	0	2	0	2
Ossific nucleus present	26	3	0	0	0	3
Closed reduction*	112
Ossific nucleus absent	48	1	0	2	0	3
Ossific nucleus present	64	0	0	1	0	1

Add to My JBJS

TABLE III PREVALENCE OF ISCHEMIC NECROSIS BY TYPE OF REDUCTION

	No. of Hips	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				Total
I	II	III	IV
Open reduction*	41
Ossific nucleus absent	15	0	0	2	0	2
Ossific nucleus present	26	3	0	0	0	3
Closed reduction*	112
Ossific nucleus absent	48	1	0	2	0	3
Ossific nucleus present	64	0	0	1	0	1

Materials and Methods

Introduction | Materials and Methods | Results | Discussion | References

We retrospectively reviewed the medical records at our two tertiary-care children's hospitals to identify patients who had been managed for congenital dysplasia of the hip during a fifteen-year period from January 1, 1979, to December 31, 1993. This review was completed by two of us (S. J. L. and G. S. B.), neither of whom had been involved in the original evaluation and management of these patients. We identified all patients who had had closed or open reduction of a congenitally dislocated hip when they were less than two years of age. Patients were excluded if their radiographs or medical records were inadequate, if they had had a previous operative attempt at closed or open reduction at another hospital, or if the dislocation of the hip was secondary to neuromuscular causes or was a teratological dislocation. The minimum duration of follow-up was three years after definitive reduction as most ischemic necrosis is usually detectable radiographically within the first two years after reduction^3,8,12,46. Patients who had been previously managed with a Pavlik harness were included in this analysis.

We identified 124 patients (153 hips) who met the criteria for inclusion. There were seven boys and 117 girls. The mean age at the time of reduction was eleven months (range, one to twenty-four months). Eighty-four hips were in patients who were less than twelve months old at the time of reduction, and sixty-nine hips were in patients who were more than twelve months old. Ninety-five patients had unilateral involvement (twenty-one right and seventy-four left hips), and twenty-nine had bilateral involvement. Twenty-five (16 percent) of the 153 hips had been previously managed with a Pavlik harness. Five attending pediatric orthopaedic surgeons had been involved in all of the reductions, and they had used similar treatment algorithms and techniques.

Radiographs made at the time of reduction were examined to determine the status of the ossific nucleus (Fig. 1). The ossific nucleus had been present in ninety hips and absent in sixty-three. Postoperative radiographs were scrutinized for the signs of ischemic necrosis as described by Salter et al.⁴⁰, and the hips that had necrosis were classified according to the criteria of Bucholz and Ogden⁴ (Fig. 2). According to Bucholz and Ogden, type-I necrosis represents a temporary, generalized delay in the development of the physeal contours and the epiphyseal ossification centers, resulting in a slight-to-mild loss of height of the epiphysis. Gage and Winter¹⁵ considered these radiographic changes to be a mild form of avascular necrosis, whereas Salter et al.⁴⁰ did not consider them to be representative of avascular necrosis. Salter et al. believed that the radiographic changes of temporary irregular ossification occurred as a result of accelerated healing secondary to the stimulation of growth after reduction. Because of confusion as to the nature and importance of the Bucholz and Ogden type-I pattern of necrosis, we analyzed our data with type-I changes considered as both positive and negative indicators of ischemic necrosis. Isolated coxa magna (an increase of more than 15 percent in the size of the involved femoral head compared with that of the normal femoral head), without physeal abnormality or any other deformity, was not considered to be ischemic necrosis^16,32. An increase in the size of the femoral head is most likely due to hypervascularity of the proximal part of the femur after reduction²⁸, which stimulates the growth of the femoral head¹⁶.

The medical records were reviewed to determine the age of the child at the time of reduction, the method of reduction, the use of preoperative traction, concomitant operative procedures, and the need for secondary operative intervention. For those patients who had bilateral involvement, each hip was considered separately, as an independent occurrence, for the purpose of statistical analysis.

The use and duration of preoperative skin traction were dependent on multiple factors, including the age of the patient, the severity or grade of the dislocation, whether the hip was reducible clinically, and the severity of the adduction contracture of the hip, to name a few. When skin traction was used (typically for a child who was able to walk), it was accomplished with the hip in a position of less than 90 degrees of flexion with slight abduction. Wide abduction was always avoided. All closed reductions were performed with the patient under general anesthesia to allow a gentle reduction of the hip. Fluoroscopy was used to ensure a concentric, stable reduction of the hip into the acetabulum while respecting the so-called safe zone of Ramsey et al.³⁸ (the arc between the angle of abduction that can be attained comfortably and the angle that allows redislocation). Patients who had a reducible hip but limited abduction and a small safe zone (less than 30 degrees) were managed with a percutaneous adductor tenotomy. Abduction of more than 60 degrees was avoided whether or not an adductor tenotomy was performed. Arthrograms were made for hips that had an equivocal reduction or were poorly visualized with fluoroscopy. An open reduction was performed if the hip was found to be unstable when the patient was initially under anesthesia or if a previous closed reduction had failed. During open reduction, attempts were made to preserve all vessels around the hip joint, specifically the medial femoral circumflex artery. Obstacles to reduction (such as the inferior aspect of the capsule and the inferior part of the transverse acetabular ligament) were released, excised (the ligamentum teres and the pulvinar), or reflected (the limbus) to allow the femoral head to rest anatomically within the acetabulum. Reduction was confirmed with intraoperative fluoroscopy.

After the initial reduction (closed or open), all patients were managed with a one and one-half spica cast with careful molding over the posterior aspect of the greater trochanter. The hips were placed into the so-called human position described by Salter et al.⁴⁰, with the hips and knees flexed 90 degrees and the involved hip abducted within the safe zone of Ramsey et al.³⁸ (a maximum of approximately 45 to 60 degrees). Intraoperative radiographs were made for all patients in order to document the reduction of the hip in the spica cast. Computerized axial tomography, which became available after July 1986, was performed within twenty-four hours after the closed reductions in order to confirm reduction of the femoral head into the acetabulum. When the femoral head was determined to be in an adequate position, the hip was maintained in the cast for six to eight weeks. If the closed reduction was successful, a second cast generally was applied with the patient under general anesthesia and with radiographic confirmation of the reduction of the hip. When the position of the femoral head was inadequate (that is, subluxated or dislocated) at any time after the reduction, the cast was removed and a repeat reduction, generally with use of an open approach, was performed.

After removal of the cast, an abduction orthosis was applied with the hip in approximately 60 degrees of total abduction. The orthosis was worn full time, both during the day and at night, until the acetabular response, as determined on radiographs, was assessed as normalized or until a secondary operative intervention was done for the treatment of residual dysplasia. Secondary operative procedures (such as varus rotational osteotomy or redirectional pelvic osteotomy) were chosen on the basis of the age of the patient and the abnormalities of the hip.

Statistical analysis was performed with use of SAS software (Statistical Analysis System, Cary, North Carolina). The Fisher two-tailed exact test was used to assess the relationship between ischemic necrosis and nominal variables. Age was treated as a categorical variable for analysis. A p value of less than 0.05 was considered to be significant.

Results

Introduction | Materials and Methods | Results | Discussion | References

The primary reduction was closed in 136 (89 percent) of the 153 hips and open in seventeen (11 percent). The primary closed reduction was successful in 112 hips (82 percent). The remaining twenty-four hips (18 percent) redislocated or subluxated, and all of them subsequently had an open reduction. The primary open reduction was successful in fifteen of the seventeen hips. Of the forty-one open reductions (seventeen primary and twenty-four secondary) that were performed, thirty-five were done through an anterolateral approach and six were done through an anteromedial approach. Four of the forty-one hips subsequently subluxated, and all four had a successful repeat open reduction.

Preoperatively, skin traction was used for 114 hips for a mean of fourteen days. At the time of the primary reduction, 110 hips had a concomitant operative procedure: ninety-nine had an adductor tenotomy, five had a varus rotational osteotomy of the proximal part of the femur, and six had both. The mean duration of immobilization in the spica cast was twelve weeks (range, six to twenty-two weeks). The mean age at the latest follow-up examination was eight years (range, three years and four months to seventeen years and ten months), and the mean duration of follow-up after the reduction was seven years and two months (range, three years to sixteen years and one month).

The prevalence of ischemic necrosis was 6 percent (nine of 153 hips) when the Bucholz and Ogden⁴ type-I hips were included (Table I). Four hips had type-I and five had type-III necrosis (Fig. 2). Ischemic necrosis occurred in four (4 percent) of the ninety hips that had an ossific nucleus at the time of reduction and in five (8 percent) of the sixty-three hips in which the ossific nucleus was absent.

If type-I changes are considered negative for necrosis of the femoral head, ischemic necrosis (types II, III, and IV) occurred in only five (3 percent) of the entire group of 153 hips (Table I). Ischemic necrosis developed in one (1 percent) of the ninety hips that had an ossific nucleus at the time of the reduction and in four (6 percent) of the sixty-three hips that had been reduced before the appearance of an ossific nucleus. Of these five hips, three were in patients who had unilateral involvement and two were in patients who had bilateral involvement.

The Fisher two-tailed exact test was used to determine if there was an association between the presence or absence of the ossific nucleus and the prevalence of ischemic necrosis. Because there is a question as to whether Bucholz and Ogden⁴ type-I changes are indicative of ischemic necrosis, the data were analyzed with type-I changes considered as both a positive and a negative indicator of ischemic necrosis. When the type-I changes were considered to be positive for ischemic necrosis, the p value was 0.489. When the type-I changes were considered to be negative for necrosis, the p value was 0.160 (Table II). A power analysis determined that our sample size was too small to detect a difference of as little as 10 percent between the prevalences of ischemic necrosis associated with the presence and absence of an intact ossific nucleus at the time of reduction of a congenitally dislocated hip. In order to achieve a reasonable power (a power of 0.80 and an alpha of 0.05) to detect a difference of 10 percent (for example, 5 percent compared with 15 percent) in the prevalence of ischemic necrosis, a sample size of 320 hips, equally divided between the two groups, would be required. However, our sample size was sufficient to achieve an excellent power (0.90) to enable detection of a difference of 20 percent (for example, 5 percent compared with 25 percent) in the prevalence of ischemic necrosis between these two groups—that is, the prevalence of ischemic necrosis in the hips reduced before the appearance of the ossific nucleus was not 20 percent higher than that in the hips reduced after the appearance of the ossific nucleus.

We analyzed the other measured variables with respect to the prevalence of ischemic necrosis (Table II). Only one variable, the type of reduction (closed or open), came close to achieving significance. When type-I changes⁴ were considered to indicate necrosis, the prevalence of necrosis after successful closed reduction was 4 percent (four of 112 hips), whereas the prevalence after open reduction was 12 percent (five of forty-one hips) (p = 0.059). However, when type-I changes were considered to be a negative indicator of necrosis, the prevalence of ischemic necrosis decreased to 5 percent (two of forty-one hips) after open reduction compared with 3 percent (three of 112 hips) after closed reduction (p = 0.611). With the numbers available, we could detect no association between a higher risk of ischemic necrosis and bilateral involvement (compared with unilateral involvement) or previous treatment with a Pavlik harness. We also could not detect an association between a lower risk of necrosis and the use of preliminary traction or the performance of an adductor tenotomy at the time of closed reduction (Table II). Finally, we could not detect a relationship between the presence or absence of the ossific nucleus and the occurrence of ischemic necrosis in the hips that had had a closed (p = 0.312) or an open (p > 0.99) reduction (Table III).

Fewer femoral and pelvic osteotomies were performed in the patients who had the reduction of the hip before the appearance of an ossific nucleus. Of the sixty-three hips that were reduced before the development of an ossific nucleus, fifteen (24 percent) had an osteotomy. Two varus rotational osteotomies were performed during the initial open reduction, and thirteen osteotomies (twelve varus rotational and one redirectional pelvic osteotomy) were done as secondary procedures for the treatment of residual acetabular dysplasia. In contrast, thirty-nine (43 percent) of the ninety hips that were reduced after the appearance of an ossific nucleus had a total of forty-five osteotomies. Nine hips had a varus rotational osteotomy at the time of the initial open reduction, and thirty hips had a total of thirty-six reconstructive osteotomies performed as secondary procedures for the treatment of residual dysplasia at a later age. The reconstructive osteotomies included redirectional pelvic osteotomies (seven hips), varus rotational femoral osteotomies (seventeen hips), and combined pelvic and femoral osteotomies (six hips).

Discussion

Introduction | Materials and Methods | Results | Discussion | References

In 1969, Salter et al.⁴⁰ implicated the use of extreme positions of immobilization (such as the so-called frog-leg position, with 90 degrees of abduction) after reduction of a congenitally dislocated hip as an etiological factor in the development of iatrogenic ischemic necrosis of the femoral head. Their findings and recommendations have been supported by numerous clinical investigations and studies of animals^{3,11,15,17,18,24,28,31,34,35,41,43,49,50,52}. Since then, other investigators have identified factors that are considered to be potentially important in the prevention of ischemic necrosis. These factors include the proper use of the Pavlik harness^25,36, maintenance of abduction within the safe zone of Ramsey et al.³⁸, the use of preoperative traction^{3,9,10,15,18,21,25,40,49,50}, adjuvant adductor tenotomy at the time of the reduction^21,40,49, emphasis on gentle reduction with the patient under general anesthesia^{3,9,10,15,18,21,24,25,41,49}, the use of femoral shortening^1,26,27,42, attention to the anatomy of the limbus¹³, and appreciation of the blood supply to the immature femoral head^{6,28,33,41,43,48}. However, even with advances in the understanding of the potential causes of iatrogenic ischemic necrosis, this sequela remains a problem as rates of ischemic necrosis of as high as 60 per cent (ninety-one of 152) have been reported after the treatment of congenital dysplasia of the hip^1,29.

In a recent report by Segal et al.⁴⁴, the absence of an ossific nucleus was defined as a potential risk factor for the development of ischemic necrosis after reduction. In that study, in which all of the patients were less than one year of age when the hip was reduced, osteonecrosis developed in one (4 percent) of twenty-five hips that had had an intact ossific nucleus compared with seventeen (53 percent) of thirty-two hips that had been reduced before the appearance of an ossific nucleus. This difference was significant (p < 0.001). However, the severity of the necrosis was not reported so it is not known if the investigators included Bucholz and Ogden⁴ type-I changes in their analysis. Their findings led them to hypothesize that the ossific nucleus has a protective effect against the development of ischemic necrosis. On the basis of the findings in previously reported anatomical studies^6,34,48, they attributed this effect to the change in the blood supply, after the beginning of ossification, from a terminal endarterial pattern to an endarterial anastomotic network, which eliminates areas of potentially tenuous blood flow within the femoral head.

Alternatively, a biomechanical explanation for the differences noted in the prevalence of ischemic necrosis between hips that had an intact ossific nucleus at the time of reduction and those that did not was recently proposed in another report by Segal et al.⁴⁵. Those investigators subjected the proximal parts of porcine femora to compressive loads. They determined that the mechanical stiffness of the femoral head increases as the size of the ossific nucleus increases. They hypothesized that an intact ossific nucleus may protect the femoral head from compressive ischemic injury after the reduction of a congenitally dislocated hip⁴⁵. Limitation of deformation of the femoral head may minimize the amount of vascular impairment within the femoral head, thereby limiting any potential ischemic injury. In vivo, both of these factors—that is, the changing patterns of the blood supply and the decreased deformation of the femoral head—may play an interactive role in preventing the development of ischemic necrosis in the immature hip. These investigations by Segal et al. suggest that delaying the reduction of a dislocated hip until the ossific nucleus is visualized on planar radiographs may have a protective effect against the development of ischemic necrosis.

To our knowledge, the study by Segal et al.⁴⁴ is the only one in which the role of the ossific nucleus in the development of ischemic necrosis of the femoral head has been directly examined, although it has been indirectly examined in analyses involving the age of the patient as the independent variable. However, a purely chronological breakdown by the age of the patients causes problems. Regardless of the age cutoff that is used, both groups will contain some patients who have an ossific nucleus and some who do not. A review of the literature shows that there is no consensus as to the importance of age in the pathogenesis of ischemic necrosis. Some reports have shown an increased risk for ischemic necrosis in younger children, specifically those who are less than three months old^22,50, those who are less than six months old^18,25,40, and those who are less than one year old³³. Some investigators have reported that older children have an increased risk for ischemic necrosis^14,15,24,29, whereas others have reported that age is of no importance in the development of ischemic necrosis^1,2,47.

We recognize several potential problems with our study. One issue is its size. We evaluated the prevalence of ischemic necrosis in 153 hips, sixty-three of which did and ninety of which did not have an ossific nucleus at the time of reduction. The prevalence of ischemic necrosis, including type I, was 6 percent (nine) in the overall series of 153 hips: 8 percent (five) of the sixty-three hips in which the ossific nucleus was absent and 4 percent (four) of the ninety hips in which it was present. The prevalence was even lower if type-I changes were considered a negative indicator of ischemic necrosis. Nevertheless, even if we consider type-I changes as indicative of necrosis, the prevalence of ischemic necrosis in the hips in our series that were reduced before the appearance of an ossific nucleus is much smaller than the prevalence of 53 percent (seventeen of thirty-two hips) identified by Segal et al.⁴⁴. With the number of patients and hips available for the present study, we were able to exclude the possibility of a difference of 20 percent between the two groups in our series. As previously indicated, a much larger sample size would have been required to identify smaller differences in the prevalence of ischemic necrosis between the groups. A multicenter study, which would have increased the number of hips in our series, could have been performed, but it would have introduced important variability in the methods of treatment. We will continue to follow, over the long term, all of the patients in the present study, and we plan to continue to add patients to our database as they meet the criteria for inclusion.

Another potential problem with our investigation is the heterogeneous nature of the study group with regard to variables such as age at the time of reduction, previous treatment (the use of the Pavlik harness), the use of traction, and the type of reduction. Our inclusion of both open and closed reductions is supported by the literature as differences have not been noted between them with respect to the development of ischemic necrosis^25,37,47. We detected no significant difference, with the numbers available, between open and closed reductions, especially when type-I patterns of ischemic necrosis were considered to be a negative indicator for necrosis: 5 percent (two) of the forty-one open reductions and 3 percent (three) of the 112 closed reductions were followed by the development of ischemic necrosis. The inclusion of patients who had been previously managed with a Pavlik harness, regardless of whether they had been managed at one of our institutions or at an outside facility, may have introduced error into our analysis. This inclusion was deemed valid because treatment with a Pavlik harness is thought to be relatively safe as it contributes only slightly or not at all to the development of ischemic necrosis^19,25,38,47. However, use of the Pavlik harness was implicated in one study as a cause of ischemic necrosis because of overly vigorous tightening of the posterior abduction strap²². When we analyzed use of the Pavlik harness independently, we did not find a significant association, with the numbers available, with the development of ischemic necrosis. However, the patients who were not managed with a Pavlik harness were generally older at the time of reduction. Hence, a comparison of the two groups may be inaccurate since the variables may not be independent.

Analysis of preoperative, intraoperative, and postoperative factors in our patients did not reveal any relevant variables with respect to the prevalence of ischemic necrosis. The use of preoperative traction has been found to be of value by some investigators^{3,15,21,23,30} but not by others^7,24,51. Analysis of our data neither supports nor negates the use of preoperative traction for the prevention of ischemic necrosis. In our series, most older children who were able to walk were managed with traction, whereas those who were younger and not able to walk generally were not. The use of traction was not rigidly controlled in this series, and statements regarding its efficacy must be understood within the context of a retrospective review of the medical records. Similarly, the addition of an adductor tenotomy at the time of reduction was not associated with a lower rate of ischemic necrosis. The use of adductor tenotomy has been reported to decrease the rate of ischemic necrosis^21,40 or to have no effect²⁴. Cadaveric studies have shown that adductor tenotomy improves blood flow to the femoral head³⁰ while increasing the amount of abduction of the hip. We liberally apply this technique to increase the safe zone of Ramsey et al.³⁸ when it is excessively narrow (less than 30 degrees). In the present study, for instance, ninety-nine (65 percent) of the 153 hips had an adjuvant adductor tenotomy at the time of reduction.

The duration of follow-up in our study, which was at least three years (mean, seven years) after definitive reduction, is a possible problem with regard to the recognition of ischemic necrosis. Ischemic necrosis is usually radiographically detectable within the first two years after reduction. However, several investigators have emphasized that certain radiographic signs of ischemic necrosis, such as lateral physeal arrest (Bucholz and Ogden⁴ type II), may not be detected until the patient is twelve years of age or older^4,25,29. The mean age at the time of the latest follow-up in our series was eight years (range, three years and four months to seventeen years and ten months). Therefore, to account for the potential development of ischemic necrosis in all of the hips in our study, we need to follow all of the patients until they have reached skeletal maturity. The low prevalence of ischemic necrosis in our patients may increase with a longer duration of follow-up. This same criticism with regard to the duration of follow-up may be leveled against the series reported by Segal et al.⁴⁴, in which the patients who had ischemic necrosis and those who did not were followed for a mean of sixty-two and thirty-six months, respectively.

With the numbers available, we did not detect any significant difference in the prevalence of ischemic necrosis between the patients who had had an intact ossific nucleus at the time of reduction and those who had not. Given the low rates of necrosis identified in both groups and in the series as a whole, we did not find any compelling reason to delay treatment of a congenitally dislocated hip on the basis of the presence or absence of an ossific nucleus. If a dislocated hip is not reduced until the ossific nucleus appears, the delay could be notable, which could have a negative impact on acetabular remodeling^37,50, necessitating additional reconstructive procedures. Irreversible changes of the acetabular and proximal femoral articular cartilage occur in congenitally dislocated hips as the patient grows older⁴³. In their long-term follow-up study of 119 patients, Malvitz and Weinstein²⁹ determined that children in whom the hip is reduced at a younger age have better radiographic and clinical outcomes. Therefore, we believe that, to avoid permanent anatomical changes in the hip joint and to optimize remodeling of the acetabulum and the proximal part of the femur, a dislocated hip should be reduced expeditiously and treatment should not be delayed until the ossific nucleus has become radiographically apparent.

References

Introduction | Materials and Methods | Results | Discussion | References

Berkeley, M. E.; Dickson, J. H.; Cain, T. E.; and Donovan, M. M.: Surgical therapy for congenital dislocation of the hip in patients who are twelve to thirty-six months old. J. Bone and Joint Surg.,66-A: 412-420, March 1984.66-A412 1984

Brougham, D. I.; Broughton, N. S.; Cole, W. G.; and Menelaus, M. B.: Avascular necrosis following closed reduction of congenital dislocation of the hip. Review of influencing factors and long-term follow-up. J. Bone and Joint Surg.,72-B(4): 557-562, 1990.72-B(4)557 1990

Buchanan, J. R.; Greer, R. B., III; and Cotler, J. M.: Management strategy for prevention of avascular necrosis during treatment of congenital dislocation of the hip. J. Bone and Joint Surg.,63-A: 140-146, Jan. 1981.63-A140 1981

Bucholz, R. W., and Ogden, J. A.: Patterns of ischemic necrosis of the proximal femur in nonoperatively treated congenital hip disease. In The Hip. Proceedings of the Sixth Open Scientific Meeting of the Hip Society, pp. 43-63. St. Louis, C. V. Mosby, 1978.

Carey, T. P.; Guidera, K. G.; and Ogden, J. A.: Manifestations of ischemic necrosis complicating developmental hip dysplasia. Clin. Orthop.,281: 11-17, 1992.28111 1992 [PubMed]

Chung, S. M. K.: The arterial supply of the developing proximal end of the human femur. J. Bone and Joint Surg.,58-A: 961-970, Oct. 1976.58-A961 1976

Coleman, S. S.: A critical analysis of the value of preliminary traction in the treatment of CDH. Orthop. Trans.,13: 180, 1989.13180 1989

Cooperman, D. R.; Wallensten, R.; and Stulberg, S. D.: Post-reduction avascular necrosis in congenital dislocation of the hip. Long-term follow-up study of twenty-five patients. J. Bone and Joint Surg.,62-A: 247-258, March 1980.62-A247 1980

Crego, C. H., Jr., and Schwartzmann, J. R.: Follow-up study of the early treatment of congenital dislocation of the hip. J. Bone and Joint Surg.,30-A: 428-442, April 1948.30-A428 1948

Esteve, R.: Congenital dislocation of the hip. A review and assessment of results of treatment with special reference to frame reduction as compared with manipulative reduction. J. Bone and Joint Surg.,42-B(2): 253-263, 1960.42-B(2)253 1960

Ferguson, A. B., Jr.: Primary open reduction of congenital dislocation of the hip using a median adductor approach. J. Bone and Joint Surg.,55-A: 671-689, June 1973.55-A671 1973

Fisher, R. L., and Cary, J. M.: Avascular necrosis complicating congenital dislocation of the hip. Course, prognosis, and orthopaedic management. Internat. Orthop.,2: 229-240, 1978.2229 1978

Fleissner, P. R., Jr.; Ciccarelli, C. J.; Eilert, R. E.; Chang, F. M.; and Glancy, G. L.: The success of closed reduction in the treatment of complex developmental dislocation of the hip. J. Pediat. Orthop.,14: 631-635, 1994.14631 1994

Fogarty, E. E., and Accardo, N. J., Jr.: Incidence of avascular necrosis of the femoral head in congenital hip dislocation related to the degree of abduction during preliminary traction. J. Pediat. Orthop.,1: 307-311, 1981.1307 1981

Gage, J. R., and Winter, R. B.: Avascular necrosis of the capital femoral epiphysis as a complication of closed reduction of congenital dislocation of the hip. A critical review of twenty years' experience at Gillette Children's Hospital. J. Bone and Joint Surg.,54-A: 373-388, March 1972.54-A373 1972

Gamble, J. G.; Mochizuki, C.; Bleck, E. E.; and Rinsky, L. A.: Coxa magna following surgical treatment of congenital hip dislocation. J. Pediat. Orthop.,5: 528-533, 1985.5528 1985

Gore, D. R.: Iatrogenic avascular necrosis of the hip in young children: a review of six cases. J. Bone and Joint Surg.,56-A: 493-502, April 1974.56-A493 1974

Gregosiewicz, A., and Wosko, I.: Risk factors of avascular necrosis in the treatment of congenital dislocation of the hip. J. Pediat. Orthop.,8: 17-19, 1988.817 1988

Grill, F.; Bensahel, H.; Canadell, J.; Dungl, P.; Matasovic, T.; and Vizkelety, T.: The Pavlik harness in the treatment of congenital dislocating hip: report on a multicenter study of the European Paediatric Orthopaedic Society. J. Pediat. Orthop.,8: 1-8, 1988.81 1988

Ilfeld, F. W., and Makin, M.: Damage to the capital femoral epiphysis due to Frejka pillow treatment. J. Bone and Joint Surg.,59-A: 654-658, July 1977.59-A654 1977

Ishii, Y., and Ponseti, I. V.: Long-term results of closed reduction of complete congenital dislocation of the hip in children under one year of age. Clin. Orthop.,137: 167-174, 1978.137167 1978 [PubMed]

Iwasaki, K.: Treatment of congenital dislocation of the hip by the Pavlik harness. Mechanism of reduction and usage. J. Bone and Joint Surg.,65-A: 760-767, July 1983.65-A760 1983

Joseph, K.; MacEwen, G. D.; and Boos, M. L.: Home traction in the management of congenital dislocation of the hip. Clin. Orthop.,165: 83-90, 1982.16583 1982 [PubMed]

Kahle, W. K.; Anderson, M. B.; Alpert, J.; Stevens, P. M.; and Coleman, S. S.: The value of preliminary traction in the treatment of congenital dislocation of the hip. J. Bone and Joint Surg.,72-A: 1043-1047, Aug. 1990.72-A1043 1990

Kalamchi, A., and MacEwen, G. D.: Avascular necrosis following treatment of congenital dislocation of the hip. J. Bone and Joint Surg.,62-A: 876-888, Sept. 1980.62-A876 1980

King, H. A., and Coleman, S. S.: Open reduction and femoral shortening in congenital dislocation of the hip. Orthop. Trans.,4: 302-303, 1980.4302 1980

Klisic, P., and Jankovic, L.: Combined procedure of open reduction and shortening of the femur in treatment of congenital dislocation of the hips in older children. Clin. Orthop.,119: 60-69, 1976.11960 1976 [PubMed]

Law, E. G.; Heistad, D. D.; Marcus, M. L.; and Mickelson, M. R.: Effect of hip position on blood flow to the femur in puppies. J. Pediat. Orthop.,2: 133-137, 1982.2133 1982

Malvitz, T. A., and Weinstein, S. L.: Closed reduction for congenital dysplasia of the hip. Functional and radiographic results after an average of thirty years. J. Bone and Joint Surg.,76-A: 1777-1792, Dec. 1994.76-A1777 1994

Mubarak, S. J.; Beck, L. R.; and Sutherland, D.: Technique. Home traction in the management of congenital dislocation of the hips. J. Pediat. Orthop.,6: 721-723, 1986.6721 1986

Nicholson, J. T.; Kopell, H. P.; and Mattei, F. A.: Regional stress angiography of the hip. A preliminary report. J. Bone and Joint Surg.,36-A: 503-510, June 1954.36-A503 1954

O'Brien, T., and Salter, R. B.: Femoral head size in congenital dislocation of the hip. J. Pediat. Orthop.,5: 299-301, 1985.5299 1985

O'Brien, T.; Millis, M. B.; and Griffin, P. P.: The early identification and classification of growth disturbances of the proximal end of the femur. J. Bone and Joint Surg.,68-A: 970-980, Sept. 1986.68-A970 1986

Ogden, J. A.: Changing patterns of proximal femoral vascularity. J. Bone and Joint Surg.,56-A: 941-950, July 1974.56-A941 1974

Ogden, J. A.: Treatment positions for congenital dysplasia of the hip. J. Pediat.,86: 732-734, 1975.86732 1975 [PubMed]

Pool, R. D.; Foster, B. K.; and Paterson, D. C.: Avascular necrosis in congenital hip dislocation. The significance of splintage. J. Bone and Joint Surg.,68-B(3): 427-430, 1986.68-B(3)427 1986

Powell, E. N.; Gerratana, F. J.; and Gage, J. R.: Open reduction for congenital hip dislocation: the risk of avascular necrosis with three different approaches. J. Pediat. Orthop.,6: 127-132, 1986.6127 1986

Ramsey, P. L.; Lasser, S.; and MacEwen, G. D.: Congenital dislocation of the hip. Use of the Pavlik harness in the child during the first six months of life. J. Bone and Joint Surg.,58-A: 1000-1004, Oct. 1976.58-A1000 1976

Robinson, H. J., Jr., and Shannon, M. A.: Avascular necrosis in congenital hip dysplasia: the effect of treatment. J. Pediat. Orthop.,9: 293-303, 1989.9293 1989

Salter, R. B.; Kostuik, J.; and Dallas, S.: Avascular necrosis of the femoral head as a complication of treatment for congenital dislocation of the hip in young children: a clinical and experimental investigation. Canadian J. Surg.,12: 44-61, 1969.1244 1969

Schoenecker, P. L.; Bitz, D. M.; and Whiteside, L. A.: The acute effect of position of immobilization on capital femoral epiphyseal blood flow. A quantitative study using the hydrogen washout technique. J. Bone and Joint Surg.,60-A: 899-904, Oct. 1978.60-A899 1978

Schoenecker, P. L., and Strecker, W. B.: Congenital dislocation of the hip in children. Comparison of the effects of femoral shortening and of skeletal traction in treatment. J. Bone and Joint Surg.,66-A: 21-27, Jan. 1984.66-A21 1984

Schoenecker, P. L.; Lesker, P. A.; and Ogata, K.: A dynamic canine model of experimental hip dysplasia. Gross and histological pathology, and the effect of position of immobilization on capital femoral epiphyseal blood flow. J. Bone and Joint Surg.,66-A: 1281-1288, Oct. 1984.66-A1281 1984

Segal, L. S.; Boal, D. K.; Borthwick, L.; Schwentker, E. P.; and Clark, M. W.: Avascular necrosis following treatment of DDH: the protective influence of the ossific nucleus. Orthop. Trans.,20: 297-298, 1996.20297 1996

Segal, L. S.; Berlin, J. M.; Schneider, D. J.; Bruno, A.; and Jacobs, C.: The contribution of the ossific nucleus to the mechanical stiffness of the capital femoral epiphysis. A porcine model for DDH. Orthop. Trans.,21: 644, 1997.21644 1997

Thomas, C. L.; Gage, J. R.; and Ogden, J. A.: Treatment concepts for proximal femoral ischemic necrosis complicating congenital hip disease. J. Bone and Joint Surg.,64-A: 817-828, July 1982.64-A817 1982

Thomas, I. H.; Dunin, A. J.; Cole, W. G.; and Menelaus, M. B.: Avascular necrosis after open reduction for congenital dislocation of the hip: analysis of causative factors and natural history. J. Pediat. Orthop.,9: 525-531, 1989.9525 1989

Trueta, J.: The normal vascular anatomy of the human femoral head during growth. J. Bone and Joint Surg.,39-B(2): 358-394, 1957.39-B(2)358 1957

Visser, J. D.: Functional treatment of congenital dislocation of the hip. Acta Orthop. Scandinavica, Supplementum 206, pp. 57-78, 1984.

Weiner, D. S.; Hoyt, W. A., Jr.; and O'Dell, H. W.: Congenital dislocation of the hip. The relationship of premanipulation traction and age to avascular necrosis of the femoral head. J. Bone and Joint Surg.,59-A: 306-311, April 1977.59-A306 1977

Weinstein, S. L., and Ponseti, I. V.: Congenital dislocation of the hip. Open reduction through a medial approach. J. Bone and Joint Surg.,61-A: 119-124, Jan. 1979.61-A119 1979

Westin, G. W.; Ilfeld, F. W.; and Provost, J.: Total avascular necrosis of the capital femoral epiphysis in congenital dislocated hips. Clin. Orthop.,119: 93-98, 1976.11993 1976 [PubMed]

Topics

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 1 Anteroposterior radiograph of the pelvis, made before reduction, in a seven-month-old child who had a dislocated right hip.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 2 Anteroposterior radiograph of the pelvis, made four years and eleven months after closed reduction of the right hip, demonstrating Bucholz and Ogden⁴ type-III involvement.

View Larger

TABLE I PREVALENCE AND CLASSIFICATION OF ISCHEMIC NECROSIS

*The values are given as the number of hips.

	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				No Evidence of Necrosis	Total
I	II	III	IV
Ossific nucleus*
Absent	1	0	4	0	58	63
Present	3	0	1	0	86	90
Total	4	0	5	0	144	153

Add to My JBJS

TABLE I PREVALENCE AND CLASSIFICATION OF ISCHEMIC NECROSIS

*The values are given as the number of hips.

	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				No Evidence of Necrosis	Total
I	II	III	IV
Ossific nucleus*
Absent	1	0	4	0	58	63
Present	3	0	1	0	86	90
Total	4	0	5	0	144	153

View Larger

TABLE II STATISTICAL ANALYSIS OF MEASURED VARIABLES WITH RESPECT TO THE PREVALENCE OF ISCHEMIC NECROSIS

*None of the findings were significant. †The ischemic necrosis was classified according to the system of Bucholz and Ogden⁴.

Factor	Types I through IV Ischemic Necrosis*†	Types II, III, and IV Ischemic Necrosis*†
Presence of ossific nucleus	p = 0.489	p = 0.160
Age at reduction
<6 mos.	p > 0.99	p > 0.99
<12 mos.	p = 0.732	p > 0.99
Unilateral compared with bilateral involvement	p > 0.99	p > 0.99
Treatment with Pavlik harness	p > 0.99	p = 0.592
Preliminary traction	p = 0.694	p = 0.602
Closed compared with open reduction	p = 0.059	p = 0.611
Adductor tenotomy	p = 0.494	p = 0.162
Varus rotational osteotomy	p = 0.685	p > 0.99
Failure of closed reduction	p = 0.150	p = 0.579
Failure of open reduction	p > 0.99	p > 0.99

Add to My JBJS

TABLE II STATISTICAL ANALYSIS OF MEASURED VARIABLES WITH RESPECT TO THE PREVALENCE OF ISCHEMIC NECROSIS

*None of the findings were significant. †The ischemic necrosis was classified according to the system of Bucholz and Ogden⁴.

Factor	Types I through IV Ischemic Necrosis*†	Types II, III, and IV Ischemic Necrosis*†
Presence of ossific nucleus	p = 0.489	p = 0.160
Age at reduction
<6 mos.	p > 0.99	p > 0.99
<12 mos.	p = 0.732	p > 0.99
Unilateral compared with bilateral involvement	p > 0.99	p > 0.99
Treatment with Pavlik harness	p > 0.99	p = 0.592
Preliminary traction	p = 0.694	p = 0.602
Closed compared with open reduction	p = 0.059	p = 0.611
Adductor tenotomy	p = 0.494	p = 0.162
Varus rotational osteotomy	p = 0.685	p > 0.99
Failure of closed reduction	p = 0.150	p = 0.579
Failure of open reduction	p > 0.99	p > 0.99

View Larger

TABLE III PREVALENCE OF ISCHEMIC NECROSIS BY TYPE OF REDUCTION

	No. of Hips	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				Total
I	II	III	IV
Open reduction*	41
Ossific nucleus absent	15	0	0	2	0	2
Ossific nucleus present	26	3	0	0	0	3
Closed reduction*	112
Ossific nucleus absent	48	1	0	2	0	3
Ossific nucleus present	64	0	0	1	0	1

Add to My JBJS

TABLE III PREVALENCE OF ISCHEMIC NECROSIS BY TYPE OF REDUCTION

	No. of Hips	Type of Ischemic Necrosis According to Classification System of Bucholz and Ogden⁴				Total
I	II	III	IV
Open reduction*	41
Ossific nucleus absent	15	0	0	2	0	2
Ossific nucleus present	26	3	0	0	0	3
Closed reduction*	112
Ossific nucleus absent	48	1	0	2	0	3
Ossific nucleus present	64	0	0	1	0	1