At birth, infants who are mildly to moderately SGA appear smaller than normal with decreased subcutaneous fat. More severely affected infants may present with a wasted appearancewith asymmetrical findings, including larger heads for the size of the body (central nervous system sparing), widened anterior fontanelles, small abdomen, thin arms and legs, decreased subcutaneous fat, dry and redundant skin, decreased muscle mass, and thin (often meconium-stained) umbilical cord. Gestational age is often difficult to assess when based on physical appearance and perceived advanced neurologic maturity. Physical examination should detail the presence of dysmorphic features, abnormal extremities, or gross anomalies that might suggest underlying congenital malformations, chromosomal defects, or exposure to teratogens. Hepatosplenomegaly, jaundice, and skin rashes in addition to ocular disorders,
Age (young and advanced) Cigarette smoking Genetics (short stature, weight) Illnesses during pregnancy (preeclampsia, severe diabetes, chronic hypertension, connective tissue disease) Infections (intrauterine) Lack of good prenatal care Oligohydramnios Poor nutrition Race (African American)
Chromosomal abnormality and nonchromosomal syndromes Congenital infections Inborn errors of metabolism Multiple gestations Insulin resistance or reduced insulin or insulin-like growth factor-1
Antimetabolites (methotrexate) Heavy metals (mercury, lead) Hydantoin Narcotics (morphine, methadone) Steroids (prednisone) Substance and illicit drug use (alcohol, cocaine) Warfarin such as chorioretinitis, cataracts, glaucoma, and cloudy cornea, suggest the presence of a congenital infection or inborn error of metabolism. Infants with severe IUGR or SGA, particularly in conjunction with fetal distress, may have problems at birth that include respiratory acidosis, metabolic acidosis, asphyxia, hypoxemia, hypotension, hypoglycemia, polycythemia, meconium aspiration syndrome, and persistent pulmonary hypertension of the newborn.
Management of IUGR and SGA infants is usually symptomatic and supportive. The diagnostic evaluation at birth should be directed at identifying the cause of the IUGR and SGA, if possible. The consequences of IUGR and SGA depend on the etiology, severity, and duration of growth retardation. The mortality rates of infants who are severely affected are 5 to 20 times those of infants who are appropriate for gestational age. Postnatal growth and development depend in part on the etiology, the postnatal nutritional intake, and the social environment. Infants who have IUGR and SGA secondary to congenital infection, chromosomal abnormalities, or constitutional syndromes remain small throughout life. Infants who have growth inhibited late in gestation because of uterine constraints, placental insufficiency, or poor nutrition have catch-up growth and, under optimal environmental conditions, approach their inherited growth and development potential.
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Hydrops fetalis is caused by immune and nonimmune conditions. Hydrops fetalis is a fetal clinical condition of excessivefluid accumulation in the skin and one or more other bodycompartments, including the pleural space, peritoneal cavity,pericardial sac, or placenta with resultant high morbidity andmortality. Hydrops initially was described in association withRhesus blood group isoimmunization. The use of Rho (D)immune globulin has reduced the incidence of isoimmune fetalhydrops. Concurrently the incidence of nonimmune hydropshas increased as a cause of this severe clinical condition.