title: The effect of intraumbilical fetal nutrition via a subcutaneously implanted port system on amino acid concentration by severe IUGR human fetuses.
abstract: OBJECTIVE
  To determine if intrauterine intraumbilical supplementation with amino acids (AA) and glucose can improve neonatal outcome of severe growth restricted human fetuses (IUGR).
  
  
  METHODS
  Prospective pilot study of intrauterine treatment of severe IUGR fetuses [n=14, 27 weeks of gestation (range 23-31)] with cerebroplacental ratio <1, with long-term intraumbilical AA and glucose supplementation (10% of feto-placental blood volume/day) using a perinatal port system alone (n=5) or combined with hyperbaric oxygenation (n=1, HBO) vs. control group (n=8).
  
  
  RESULTS
  The duration of continuous intraumbilical AA/glucose supplementation was 11 (6-13) days. Daily intravascular fetal nutrition significantly prolonged the brain sparing to delivery interval by 24 (14-33) days vs. 5.6 (2-12) days in controls. Fetal nutrition reduced blood flow resistance in the placental circulation but did not affect the Doppler profile of cerebral arteries. Higher weight gain of 113.5 (36-539) g was observed following supplementation compared to 33.3 (8-98) g in the control group (P<0.05). In spite of this, fetuses below 28 weeks of gestation did not sufficiently benefit from infused commercial AA. We found a reduced fetal plasma concentration of the essential AA histidine, threonine, lysine and arginine, and non-essential AA taurine, in severe IUGR fetuses in both groups. Long-term supplementation with a commercial AA formula led to a slight, but not significant, reduction of histidine, threonine, lysine, arginine, asparagine and glutamine. However, the concentration of tryptophan and glutamic acid slightly increased. HBO can be combined with AA supplementation via a port system. In one case, the port system was also successfully used for fetal blood transfusion.
  
  
  CONCLUSIONS
  Intravascular treatment of IUGR with fetal nutrition can prolong pregnancy with severe placental insufficiency and brain sparing for many weeks. However, rather than normalizing AA concentrations, an enhanced AA imbalance was observed in IUGR fetuses following supplementation. These deviations in AA concentrations prevent the recommendation for use of commercial AA solutions for prenatal treatment of extreme preterm IUGR fetuses.
authors.forename: Michael
authors.initials: M
authors.lastname: Tchirikov
authors.forename: Zhaxybay Sh
authors.initials: ZS
authors.lastname: Zhumadilov
authors.forename: Gauri
authors.initials: G
authors.lastname: Bapayeva
authors.forename: Michael
authors.initials: M
authors.lastname: Bergner
authors.forename: Michael
authors.initials: M
authors.lastname: Entezami
mesh_terms: D000328:Adult; D000596:Amino Acids / Q000008:administration & dosage; D002405:Catheterization, Central Venous / Q000379:methods*; D005260:Female; D005317:Fetal Growth Retardation / Q000628:therapy*; D046128:Fetal Therapies / Q000379:methods*; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D010288:Parenteral Nutrition / Q000379:methods*; D010865:Pilot Projects; D010927:Placental Insufficiency; D011247:Pregnancy; D011446:Prospective Studies; D014471:Umbilical Veins; D062666:Vascular Access Devices; D055815:Young Adult
chemical_list: D000596:Amino Acids; D005947:Glucose