**4. Fragility neonatal fractures**

Fractured neonatal femur may be the initial sign of an underlying disease with bone fragility. Osteogenesis imperfecta (OI) is a heterogeneous connective tissue disorder characterized from severe osteoporosis. The synthesis of collagen type I is disrupted due to pathogenic genes. There is low bone mass with bone fragility that leads to recurrent fractures of the axial skeleton and the long bones resulting in severe deformities. Although there have been reported to be more than 20 types of gene

#### **Figure 11.**

*Minimal incision, release of muscles and reduction, stabilized with a K-wire and hip spica. Apparent callus formation in a week time after reduction.*

heterogeneity of OI, the clinical phenotype classification of Silence remains a valuable description of the severity of the disorder. The lethal form (type 2) presents with intrauterine fractures diagnosed with the prenatal ultrasonography. Long bones are described with bowing and shortening. X-ray examination in the neonate reveals several fractures, occasionally affecting the ribs as well. Femoral or tibial fractures are either spiral or transverse fractures. Type 3 OI presents with fractures without history of urgent manipulation of the neonate because of dystocia. On x-ray examination the bones are deformed and there is cortical thinning [26–28] (**Figure 12**).

With minor handling of the neonate, a crack may be felt and a new fracture may be diagnosed. There are clinical features with the prominent frontal bone, the short height of the neonate, and the ligamentous laxity. Child abuse must be ruled out in the presence of multiple fractures that are at different times of callus formation. Fractures found in clavicles, long bones or vertebrae are strong indications of the underlying

#### **Figure 12.**

*Initial fracture of the left femur, following an uncomplicated normal vaginal delivery. Bowing and sclerosis of the right femur is noticed. The girl was diagnosed with osteogenesis imperfecta type 3*.

### *Neonatal Fractures DOI: http://dx.doi.org/10.5772/intechopen.110167*

bone fragility [29]. There are several metabolic diseases affecting the neonate that present with neonatal fractures. Disturbances of the calcium and phosphate metabolism as in phosphatasia and rickets are among the rare but severe diseases that are diagnosed through neonatal fractures, affecting both long bones and vertebrae and ribs. Appropriate laboratory investigations from neonatologists and endocrine pediatricians with genetic investigations, can provide an accurate diagnosis [30–34]. Treatment of neonatal fractures that are due to metabolic diseases follows the same principles as the femoral fractures of normal neonates with the use of Gallows traction. Modifications for use of traction in the neonatal box are described. Appropriate medical treatment is essential in order to reduce the number of fractures that may follow. Gene therapy is today the most promising treatment method for these severe forms. Stem cells therapy in the prenatal period has been reported [35].

Bilateral neonatal femoral fractures have been reported in a neonate with multiple congenital anomalies, with joint stiffness, similar to arthrogryposis. Arthrogryposis may be prenatally detected in a fetus with reduced mobility. It is important for the obstetrician to be informed of the joint stiffness in order to avoid vigorous movements that may lead to neonatal fractures [36] (**Figures 13** and **14**).

**Figure 13.**

*Bilateral fractured femur in a neonate with complex stiff joints. Casts were applied for the club feet deformities. Treatment provided with Gallows traction. X-ray with united femoral fractures.*

#### **Figure 14.**

*Bilateral fractured femur in a neonate with complex stiff joints. Casts were applied for the club feet deformities. Treatment provided with Gallows traction. X-ray with united femoral fractures.*
