Atypical Musculoskeletal Growth and Motor Development

CHAPTER 2

Atypical Musculoskeletal Growth and Motor Development

Atypical Musculoskeletal Growth

• Constitutional growth delay: Weight and height decrease toward the end of infancy, remain below family pattern but with stable growth velocity during middle childhood, and then increase toward the end of adolescence, resulting in normal adult stature. Bone ages are typically delayed, and there is often a family history of delayed growth (“late bloomer”).

• Familial short stature: The child and parents are small, and the child’s growth remains below but parallels the normal curves.

— There is a risk of overdiagnosing or underdiagnosing atypical growth findings in children with extremely tall or short parents if parental height is not taken into account. Midparental height can be used to estimate genetic potential for height.

• When examining growth, most children and adolescents track between one or 2 growth percentiles. Deviation from this warrants additional consideration and possible evaluation.

• Appropriate nutrition is the critical environmental factor that supports normal biological maturation; adequate food intake supports normal weight gain and linear growth.

NUTRITIONAL CAUSES

• Failure to thrive: Exact definition varies, but generally considered to be weight less than the fifth percentile or weight percentile that declines more than 2 major percentile lines (eg, declines from the 80th percentile to the 40th percentile).

• Undernutrition: Weight for age typically declines (wasting) before height for age (stunting) and weight for height (or body mass index).

— Undernutrition is often associated with delay in skeletal maturity relative to chronological age and delay in attainment of peak height velocity and pubertal development.

• Obesity and overweight are often associated with advanced maturation, including growth and pubertal development, although in adolescent males they can be associated with delayed pubertal development.

NON-NUTRITIONAL CAUSES

• Non-nutritional causes of atypical growth include genetic causes, endocrine conditions, infection, trauma, and tumors.

• Growth plate injuries and metabolic disorders (eg, rickets) can inhibit growth.

• Inflammatory disorders or trauma may damage the growth plate or articular cartilage and result in malunion, shortening, or angular deformity.

• Pituitary tumors, chronic osteomyelitis, foreign body reaction, and some fractures may accelerate growth.

• Non-nutritional causes affect weight and length in different ways than nutritional causes.

— Genetic causes (eg, skeletal dysplasias) tend to affect weight and length symmetrically.

— Endocrine causes (eg, hypothyroidism, Cushing syndrome, growth hormone deficiency) tend to affect length more than weight.

CONGENITAL GROWTH DEFECTS

• Musculoskeletal problems account for about one-third of congenital defects, with hip dysplasia and clubfoot accounting for half of the primary musculoskeletal defects.

• Three percent of newborns have major defects, that is, those that are life-threatening, require major surgery, or cause significant disability.

• Infants with multiple minor defects (eg, syndactyly of toes 2 and 3, single transverse palmar crease) should be thoroughly evaluated to exclude a major malformation.

• Atypical morphogenesis can be classified into 4 categories of defects: malformations, disruptions, deformations, and dysplasias.

— Malformations, such as limb hypoplasia, arise during organogenesis and are of teratogenic or genetic origin.

— Disruptions, such as amniotic band sequence, occur later in gestation when teratogenic, traumatic, or other factors interfere with normal fetal growth. These are less likely to be inherited.

— Deformations, such as calcaneovalgus foot deformity, occur at the end of gestation and are caused by intrauterine crowding or position.

— Dysplasias, such as achondroplasia, result from altered growth that occurs before and after birth.

• Developmental variations, which may resolve with time and seldom require any treatment, should be differentiated from deformities. Examples discussed elsewhere in this book include flatfoot (Chapter 52), in-toeing (Chapter 24), out-toeing (Chapter 25), and genu valgum (knock knee) or genu varum (bowleg) (Chapter 26, Angular Deformities).

—

Only gold members can continue reading. Log In or Register to continue