Adverse neonatal and pediatric effects occur with maternal alcohol consumption during pregnancy. The diagnosis of fetal alcohol syndrome (FAS) is based on findings in the following 3 areas: (1) characteristic facial anomalies, (2) growth retardation (intrauterine growth restriction and failure to have catch-up growth), and (3) CNS involvement (cognitive impairment, learning disabilities, or behavioral abnormalities).
renatal exposure to alcohol is associated with a variable spectrum of effects referred to as fetal alcohol spectrum disorders (FASD), with fetal alcohol syndrome at the most severe end of that spectrum. Children with fetal alcohol syndrome disorder may have clinically significant CNS involvement but few or no characteristic physical features.

Pathophysiology

Alcohol crosses the placenta and rapidly reaches the fetus. Extensive studies have demonstrated equivalent fetal and maternal alcohol concentrations, suggesting an unimpeded bidirectional movement of alcohol between the 2 compartments. The fetus appears to depend on maternal hepatic detoxification because the activity of alcohol dehydrogenase (ADH) in the fetal liver is less than 10% of that observed in the adult liver. Furthermore, the amniotic fluid acts as a reservoir for alcohol, prolonging fetal exposure.

The mechanism for the spectrum of adverse effects on virtually all organ systems of the developing fetus is unknown. Ethanol and its metabolite acetaldehyde can alter fetal development by disrupting cellular differentiation and growth, disrupting DNA and protein synthesis and inhibiting cell migration. Both ethanol and acetaldehyde modify the intermediary metabolism of carbohydrates, proteins, and fats. Both also decrease the transfer of amino acids, glucose, folic acid, zinc, and other nutrients across the placental barrier, indirectly affecting fetal growth due to intrauterine nutrient deprivation. Elevated levels of erythropoietin in the cord blood of newborns exposed to alcohol are reported and suggest a state of chronic fetal hypoxia.
source:emedicine.medscape.com/article/974016-diagnosis

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Patent ductus arteriosus (PDA) is a persistence of the fetal connection (ductus arteriosus) between the aorta and pulmonary artery after birth, resulting in a left-to-right shunt. Symptoms may include failure to thrive, poor feeding, tachycardia, and tachypnea. A continuous machine-like murmur in the upper left sternal border is common. Diagnosis is by echocardiography. Administration of indomethacin with or without fluid restriction may be tried in premature infants with a significant shunt but not in term infants with PDA. If the connection persists, surgical or catheter-based correction is indicated. Endocarditis prophylaxis is recommended before and for 6 to 12 mo after correction.

can we used indomethacine in the child after 5 months with patent ductus arteriosus ?

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A 1 month old male child presented with the history of abdominal distension associated with vomiting and recurrent chest infection and  passing  clay colored stool several episode per day since 15 days of life.On lab examination total bilirubin was 9.4gm/dl, direct bilirubin 3.2gm/dl and other liver function test revealed normal range.  On view of biliary atresia USG was done and revealed  normal.hematology revealed thrombocytopenia and other normal.The baby was treated symptomatically but the abdominal distension and clay colored stool still persisting. Anyone can give your opinion for this case?

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