IUGR

Question 1

What is IUGR? And what is the clinical significance?

Answer 1

• failure of the fetus to achieve growth potential
  
  • small for gestational age = BW <10th centile
• ST:
  
  • preterm labour
  • perinatal mortality
  • neonatal morbidity (hypothermia, infection, BSL, meconium, hypoxic ischaemic encephalopathy, poor feeding).
• LT
  
  • childhood LT morbidity - CP and ID - mostly CP is global impairment as well as motor.
  • adulthood morbidity (obesity, HTN, heart disease, DM, dyslipidemia). DOAD. developmental origins of adult disease.

Question 2

Causes of small Intrauterine growth?

Answer 2

• fetal
  
  • congenital:
    
    • chromosomal
      
      • trisomy (21, 18, 13, Klinefelters, Turners - others are lethal),
      • monosomy, deletions,
      • UPD - maternal vs paternal - in utero is clever switches on maternal and off paternal until after birth - two sets of one parent and none from the other - emergence of recessive conditions,
      • comfined placental mosaicism (in placenta chromosomal but baby is fine)
    • genetics - single gene disorders
    • structural abnormalities - gastroschisis, exomphalos, CHD, diaphragmatic hernia, skeletal dysplasia
    • familial
  • infections (T Other RCH)
    
    • toxoplasma - cat poo, litter boxes, raw meat. Stray cat does the damage - gardening/sand pit. Handwashing. Southern Europe big problem.
      
      • treatable: antitoxoplasmosis drugs.
    • CMV (hand washing) - childcare centers - clonal theory of immunogenesis (exposed at childhood don’t develop immunity to it) - CMV as fetus regard as self. Vast majority is hand to mouth.
      
      • 350 CMV a year - need vaccine. no tx. difficult against herpes viruses.
    • syphilus
  • maternal
    
    • vascular disease
      
      • 2 types of CTD - Marfan’s, collagen/elastin - EDS -ehlers danlos, SLE/rheumatoid
      • HTN - preeclampsia
      • DM
      • renal disease
    • thyroid disease (hyperthyroidism Graves - Abs cross into baby)
    • kidney
    • thrombophilia
      
      • congenital
        
        • hyperhomocystenemia 20% (diet)
        • FV leiden 5%
        • Prothrombin G 2%
        • Protein S/C - bad ones
        • antithrombin III - bad ones
          
          • placental blood vessels special. CO 5L/min. 30% to uteroplacental.
          • 6-7mins to bleed out into placenta. Acute blood loss - 30% notice, 40% dead. 35% deteriorate.
      • acquired
        
        • antiphospholipid syndrome - autoimmune, thrombosis everywhere
        • pregnancy, smoking, cancer, immobility, trauma)
    • toxins
      
      • smoking, alcohol
    • malnutrition
      
      • any
    • cardiac disease
    • anaemia
      
      • correctable causes
    • atmospheric resp hypoxia (altitude)
• placental
  
  • multiple pregnancies
  • abruption (haemorrhagic, trauma)
  • placental abnormality

Question 3

Screening of IUGR

Answer 3

• symphyseal fundal height
• USS
  
  • better than SFH
  • optimal timing at 34weeks
  • abdominal circumference - best biometric measure

Question 4

What management for fetal growth restriction?

Answer 4

• Prevention:
  
  • aspirin (high BP) - start at <16 weeks
  • rest + work optimisation
  • vit E/C doesn’t work (free radical scavengers don’t)
  • sildenafil - placental arteriolar vasodilator - may work. Major trial.
• fetal surveillance
• confirm diagnosis
• work out cause (Hx, Ex, Ix)
  
  • normal? - parental small, amniotic fluid good, physically active.
  • tertiary US
  • FBE - anaemia,
  • UEC - renal, t
  • thrombophilia,
  • NIPS
    
    • week 10-13 CVS
    • week 16-18 amniocentesis
    • Vic can terminate at 35 weeks with KCL (potassium injection). 2x in 10 years, reduced terminations.
      
      • good for waiting and seeing
      • twins
    • neonatal palliative care
    • really small baby - trisomy 18 (most important to pick up), trisomy 13
  • CMV/toxo - serology for IgM or stored at first visit.
• treat
  
  • control DM
  • rest
  • give oxygen
    
    • 760atm 21% O2
    • pO2 room air - 150mmHg - 100 for us. Dead space, rebreathing air you breathed out.
    • give mother O2 - dissolve oxygen in blood. Not much you can do.
  • optimise nutrition - poor blood flow but its richer and more nourishment
    
    • increase growth without oxygenation causes death.
  • do NOT lower BP with fixed BV narrowing
• delivery - most important, timing of birth.
  
  • corticosteroids if lung immaturity
  • will need MgSO4 <30wks - provides neuroprotection (cerebral arteriolar agent), protective risk of arteriolar vasospasm
  • CS if hypoxic

Question 5

What is the principles of management of a preterm IUGR baby?

Answer 5

• determining IUGR?
  
  • BPP - biophysical profile (tone, breathing, limbs, AFI + CTG)
  • CTG - 28 weeks can
  • Ductus venosus (measure of acidemia, heart failure through a waves)
  • umbilical artery (resitance - UAPI - pulsatility index and direction of flow (reversed or absent)
  • MCA - velocity/flow - anaemia.
• Deliver based on:
  
  • CTG - loss of variability or declerations
  • Umbilical artery reversal
  • ductus (early or late changes)
• Before delivery give:
  
  • corticosteroids (betamethasone) for:
    
    • periventricular haemorrhage prevention
    • reducing necrotising enterocolitis (NEC)
    • lung development (HMD/Neonatal ARDS)
  • magnesium sulfate (stabilises neuronal membranes - LT CP prevention)
• Caesarian/Induction.

Question 6

What are the management of a term IUGR baby? What are the options?

Answer 6

Based on the preference of the women, but delivery has better outcomes if <10% percentile for estimated weight:

• placental function
• estimated wieght
• BPP

Question 7

What factors on CTG would make you consider a delivery in an IUGR baby? What would you do for 2 requent variables with sustained bradycardia?

Answer 7

• loss of variability: 5-25 normal
  
  • 3-5 = low
  • <3 = absent
• variability has best acidemia correlation (pH of the baby)
  
  • 2 acclerations in 20mins 5back 15seconds
• declerations:
  
  • early - normal - corresponds with contractions (head compression)
  • late - slow onset, chemoreceptor mediated, every contraction
  • variable decelerations: cord compression, baroreceptor mediated
    
    • complicated (plateau at bottom related with contraction) - depth 60, length 60
    • shouldering (physiological) - peaks either side of decrease
    • late component - down plateau with slow recovery
      *

Question 8

What would you do for 2 frequent contractions followed by sustained bradycardia on a CTG? Whats the cause?

Answer 8

• causes:
  
  • hyperstimulation
  • rupture (trial of scar)
  • abruption
  • cord prolapse
• management:
  
  • VE (dilated? cord prolapse? mode?)
  • Resus (O2, IV fluids, LLD, tocolytic)
  • Surg? Induce?