short stature

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  • 1. Short stature, optimally defined relative to the genetic endowment of the individual, is recognized by comparing an individual childs height with that of a large population of a similar genetic background and, more particularly, using the mid-parental target height (see History). Growth failure (GF) is often confused with short stature. By definition, GF is a pathologic state of abnormally low growth rate over time, whereas short stature is often a normal variant. Regardless of the genetic background, short stature may be a sign of a wide variety of pathologic conditions or inherited disorders. Thus, accurate longitudinal growth assessment is a fundamental aspect of health maintenance in children. Reviewing the patient's growth chart is critical to evaluating short stature. Deviation from a prior growth pattern appropriate for the genetic background often heralds new pathology. In addition, analysis of the prior growth pattern helps distinguish normal growth from pathologic variants of short stature. Compared with a well-nourished, genetically relevant population, short stature is defined as a standing height more than 2 standard deviations (SDs) below the mean (or below the 2.5 percentile) for sex.[1] Skeletal maturation is typically determined by the bone age, which is assessed using anteroposterior radiography of the left hand and wrist. Sex-specific reference data for standing height, head circumference, and weight have been published for most developed countries, most ethnic subpopulations (including Asians and blacks), and the most common genetic disorders (eg, Down syndrome, Ullrich-Turner syndrome, achondroplasia). The causes of short stature can be divided into 3 broad categories: chronic disease (including undernutrition genetic disorders), familial short stature, and constitutional delay of growth and development. Endocrine diseases are rare causes of short stature (see Frequency). The hallmark of endocrine disease is linear GF that occurs to a greater degree than weight loss. Most short children evaluated by clinicians in developed countries have familial short stature, constitutional growth delay, or both. Short stature and constitutional growth delay are diagnoses of exclusion. The hallmarks of familial short stature (also referred to as genetic short stature) include bone age appropriate for chronologic age, normal growth velocity, and predicted adult height appropriate to the familial pattern (using the Bayley-Pinneau or Tanner-Goldstein-Whitehouse tables). By contrast, constitutional growth delay is characterized by delayed bone age, normal growth velocity, and predicted adult height appropriate to the familial pattern (see image below).

2. Constitutional growth delay: This condition describes children who are small for their ages but who are growing at a normal rate. They usually have a delayed "bone age," which means that their skeletal maturation is younger than their age in years. (Bone age is measured by taking an X-ray of the hand and wrist and comparing it with standard X-ray findings seen in kids the same age.) These children don't have any signs or symptoms of diseases that affect growth. They tend to reach puberty later than their peers do, with delay in the onset of sexual development and the pubertal growth spurt. But because they continue to grow until an older age, they tend to catch up to their peers when they reach adult height. One or both parents or other close relatives often had a similar "late-bloomer" growth pattern. Familial (or genetic) short stature: This is a condition in which shorter parents tend to have shorter children. This term applies to short children who don't have any symptoms of diseases that affect their growth. Kids with familial short stature still have growth spurts and enter puberty at normal ages, but they usually will only reach a height similar to that of their parents. With both constitutional growth delay and familial short stature, kids and families need to be reassured that the child does nothave a disease or medical condition that poses a threat to health or that requires treatment. However, because they may be short or may not enter puberty when their classmates do, some may need extra help coping with teasing or reassurance that they will go through full sexual development eventually. In a few children who are very short or very late entering puberty, hormone treatment may be helpful. 3. The families of children who fail to thrive: preliminary investigations of parental deprivation among organic and non- organic cases. Gagan RJ, Cupoli JM, Watkins AH. Abstract A majority of cases of failure to thrive (FTT) do not have a known organic etiology. Social and psychological determinants are sought for these "non-organic failure to thrive" (N-O FTT) cases. Social and psychological differences between non-organic and organic cases are also explored here. With the introduction of the term, "maternal deprivation," medical practitioners have implicated mothers' deficiencies as instrumental in the etiology of N-O FTT. However, these mothers are themselves usually deprived. Lack of cooperation in childcare by both parents is noted when classic clinical cases are reviewed. We suggest that the concept, "parental deprivation," provides a more accurate model. Preliminary research findings support our hypothesis that mothers of FTT infants do not have good social support networks. Teen motherhood and socioeconomic status also appear to be important, but not necessary as determinants. An unexpected finding is that there are few differences in the social deficiencies of families of N-O FTT infants as compared to those failing for organic reasons. Two unanticipated findings appear noteworthy. First, infants failing for organic reasons are significantly smaller and thinner at birth, independent of pregnancy complications or prematurity. Second, infants failing for non-organic reasons are more likely to present during the period of infant-caretaker role development and less likely in the later toddler stage. Additional research into the feasibility of strengthening family supports as a basis of intervention is recommended.