Avascular Necrosis (AVN) in DDH: Classification, Risk Factors, and Management

What is AVN in DDH classification?

Avascular Necrosis (AVN) in the context of Developmental Dysplasia of the Hip (DDH) refers to a severe complication of DDH treatment, characterized by the death of bone tissue in the femoral head due to an interruption of its blood supply, and is subsequently classified based on the extent of damage to guide prognosis and management.

Understanding Developmental Dysplasia of the Hip (DDH)

Developmental Dysplasia of the Hip (DDH) is a spectrum of abnormalities of the hip joint, ranging from subtle acetabular dysplasia (a shallow hip socket) to frank dislocation of the femoral head from the acetabulum. It is a common congenital condition that, if left untreated, can lead to significant pain, gait abnormalities, leg length discrepancy, and early-onset osteoarthritis in adulthood. Early diagnosis and intervention are critical for optimal outcomes, as the immature hip joint has significant remodeling potential. Treatment often involves repositioning the femoral head within the acetabulum (reduction) and maintaining this position with bracing, casting, or, in more severe cases, surgery.

What is Avascular Necrosis (AVN)?

Avascular Necrosis (AVN), also known as osteonecrosis or aseptic necrosis, is a debilitating condition resulting from the temporary or permanent loss of blood supply to an area of bone. Without adequate blood flow, bone tissue dies and collapses, leading to joint destruction. While AVN can affect various bones in the body, it is particularly devastating when it occurs in weight-bearing joints like the hip, specifically the femoral head. The femoral head's unique blood supply, primarily through the medial circumflex femoral artery, makes it susceptible to insult. When AVN affects the femoral head, the bone structure weakens, potentially leading to collapse of the articular surface, pain, and severe functional impairment.

The Critical Link: AVN as a Complication of DDH Treatment

It is crucial to understand that Avascular Necrosis is not an inherent part of Developmental Dysplasia of the Hip itself. Instead, AVN is a significant and feared complication that can arise during or after the treatment of DDH. The primary mechanism involves iatrogenic (treatment-induced) damage or compromise to the delicate blood supply of the femoral head during reduction maneuvers (whether closed or open) or prolonged immobilization in certain positions.

The immature femoral head is particularly vulnerable due to its developing blood supply. Excessive force during reduction, extreme positions of immobilization (e.g., hyperabduction), or direct surgical trauma can disrupt the crucial vessels supplying the femoral head, leading to ischemia and subsequent necrosis. The potential for AVN is a major consideration for orthopedic surgeons treating DDH, and careful technique is paramount to minimize this risk.

Classifying AVN in the Context of DDH (Salter Classification)

When AVN occurs following DDH treatment, its severity and extent are often classified to guide prognosis and further management. One of the most widely recognized classifications for AVN of the femoral head in DDH is the Salter Classification (or Salter-Thompson classification), which categorizes the damage based on radiographic findings and the involvement of the epiphyseal plate (growth plate):

• Type I: Involvement of only the secondary ossification center (the bony nucleus within the cartilage of the femoral head). The epiphyseal plate is spared. This type generally has the best prognosis.
• Type II: Involvement of the ossification center and a portion of the epiphyseal plate. This implies partial damage to the growth plate, which can lead to some growth disturbance.
• Type III: Involvement of the ossification center and total involvement of the epiphyseal plate. This is a more severe form, indicating significant damage to the growth plate, which can result in severe growth disturbances, femoral shortening, and coxa vara (a deformity where the angle between the femoral neck and shaft is decreased).
• Type IV: Involvement of the ossification center, the entire epiphyseal plate, and a portion of the metaphysis (the wider part of the bone near the growth plate). This is the most severe type, carrying the worst prognosis for normal hip development and function, often leading to significant deformity and early osteoarthritis.
• Type V (sometimes included): Complete cessation of growth of the femoral head due to premature physeal closure.

Other classification systems, such as Kalamchi and MacEwen or Bucholz and Ogden, also exist, providing similar insights into the extent of femoral head involvement and aiding in predicting long-term outcomes. The classification helps clinicians understand the potential for future deformity, the need for further intervention, and the long-term prognosis for the hip joint.

Risk Factors for AVN in DDH Treatment

Several factors can increase the risk of developing AVN following DDH treatment:

• Age at Reduction: Older children (especially those over 6-12 months) are at higher risk due to the greater forces often required for reduction and the relative maturity of the femoral head's blood supply, making it less resilient to compromise.
• Forceful Reduction Attempts: Aggressive or repeated attempts at closed reduction can traumatize the blood vessels supplying the femoral head.
• Extreme Positions of Immobilization: Maintaining the hip in positions of excessive abduction (greater than 60-70 degrees) and/or internal rotation within a cast or brace can compress blood vessels.
• Type of Reduction: Open reduction (surgical exposure of the hip joint) can sometimes carry a higher risk of direct vascular injury compared to gentle closed reduction.
• Severity of Initial DDH: More severe or irreducible dislocations may require more extensive maneuvers or surgery, increasing the risk.
• Multiple Reduction Attempts: Repeated attempts at reduction increase the cumulative risk of vascular compromise.

Clinical Implications and Management

The development of AVN significantly complicates the treatment course and long-term prognosis for patients with DDH. It can lead to:

• Femoral Head Deformity: Irregular shape and collapse of the femoral head.
• Growth Disturbances: Shortening of the femur and/or altered alignment of the hip joint.
• Early Onset Osteoarthritis: Due to the irregular joint surface and altered biomechanics.
• Pain and Functional Limitation: Restricting mobility and quality of life.

Management of AVN is complex and depends on the severity and classification type. It can range from conservative measures (e.g., bracing, activity modification) to various surgical interventions aimed at preserving the femoral head, correcting deformities, or eventually hip replacement in severe cases. Regular radiographic follow-up is essential after DDH treatment to monitor for signs of AVN.

Prevention: The Best Strategy

Given the severe consequences of AVN, prevention is paramount in DDH management:

• Gentle Reduction Techniques: Employing minimal force during closed reduction maneuvers.
• Avoiding Extreme Positions: Ensuring that casts or braces do not place the hip in positions that compromise blood flow.
• Careful Surgical Planning: Meticulous surgical technique during open reduction to protect vascular structures.
• Early Diagnosis and Intervention: Treating DDH as early as possible (ideally in infancy) often allows for less invasive and lower-risk interventions.

In summary, AVN is a critical complication in the management of DDH, necessitating careful consideration of risk factors and precise execution of treatment strategies to ensure the best possible long-term outcomes for hip health.