Saturday, August 5, 2017

- Maternal factors causing IUGR.

  Maternal factors causing Intrauterine Growth
Restriction

·     Maternal genetic factors:

-        Mothers who were growth-restricted at birth have a twofold increase in risk for FGR in their offspring.

-        Mothers who give birth to an FGR newborn are at high risk of recurrence, and the risk increases with increasing numbers of FGR births.

·     Maternal disorders reducing uteroplacental blood flow: such as preeclampsia, eclampsia, chronic renal vascular disease, and chronic hypertensive vascular disease, Autoimmune syndromes (antiphospholipid, lupus erythematosus), and pregestational diabetes often result in ↓ uteroplacental blood flow and result in FGR, Impaired delivery of oxygen and other essential nutrients is thought to limit organ growth and musculoskeletal maturation. Risk of placental thrombi is increased in conditions of inherited thrombophilia.

·     Extreme and prolonged Maternal malnutrition:

-      because changes in maternal nutrition, unless extreme and prolonged, do not markedly alter maternal plasma concentrations of nutrient substrates or the rate of uterine blood flow, the principal determinants of nutrient substrate delivery and transport to the fetus by the placenta.

-      Zinc deficiency in pregnant women has been associated with increased rates of preterm delivery and fetal IUGR.

-      Thiamine deficiency in pregnant women also has been associated with IUGR.

-      Protein restriction rather than caloric restriction before 26 weeks can cause symmetric IUGR.

-      GIT diseases: Crohn’s, ulcerative colitis, gastrointestinal bypass surgery  .

Wednesday, August 2, 2017

Sunday, July 30, 2017

- Fetal factors Causing IUGR.

 Fetal factors Causing IUGR

·     Constitutional: most of SGA infants are normal (genetically small)

·     Genetic causes (5-20%)

-        Chromosome anomalies include: Aneuploidy (like Trisomy 21, 18, 13, and 16), uniparental disomy (of chromosomes 6, 14, 16), partial deletions or duplications (Cri du chat syndrome, Wolf Hirschhorn syndrome), ring chromosome, and aberrant genomic imprinting. The finding of symmetric FGR prior to 20 weeks of gestation suggests aneuploidy as the cause, most commonly trisomy 18.

-        Single gene disorders such as Russell Silver syndrome, Bloom syndrome, Cornelia de Lange syndrome, and Fanconi anemia have been associated with FGR.

·       Congenital malformations (e.g., Cardiovascular anomalies, Congenital diaphragmatic hernia, abdominal wall defects (omphalocele and gastrochisis), renal agenesis or dysplasia, anencephaly, tracheoesophageal fistula, single umbilical artery, gastrointestinal atresia, Potter syndrome, anorectal malformation, and pancreatic agenesis)

·       Congenital infection (CMV and toxoplasmosis are the most common), the incidence is highest when infection occurs in the 1st  trimester, CMV and rubella are associated with severe FGR.

·     IEM (e.g., galactosemia and phenylketonuria).

·     Insulin deficiency (production or action of insulin)

·     Insulin-like growth factor type I deficiency

 

 

Sunday, July 23, 2017

- Ponderal index.

 

Ponderal index

The ponderal index (PI) is a useful tool to detect FGR, particularly in infants with asymmetric FGR.

PI is a ratio of body weight to length expressed as:

PI = [weight (in g) x 100] ÷ [length (in cm)]3

Ponderal index is recorded as a number in g/cm3, but there are also percentile curves for ponderal index.

Normal ponderal index is GA dependent, but is generally 2.2 to 3.0 g/cm3 (3rd and 97th percentile).

A ponderal index of <2 or <10% is abnormal and suggests asymmetrical FGR. Infants with constitutional or symmetric FGR typically have a normal ponderal index.

With normal growth, the PI increases gradually from 30 to 37 weeks gestation and then remains constant. Decreased growth of adipose tissue and skeletal muscle, the major contributors to body weight, results in a reduced PI. PI of less than the 10th percentile reflects fetal malnutrition; PI of less than the 3rd percentile indicates severe wasting.