Transcript Intrauterine Growth Retardation - MUI

Intra Uterine Growth
Retardation
Dr.B Khani MD
Case 1
 27 Y G2 L1 36 w
CC: VB & LP
PMH: Iron deficiency anemia (no treatment)
Spotting in 24 w pregnancy
 PH: The patient was pale FH: 32 cm
V /E: 4cm
The newborn birthed after 3 h
 N: female APGAR: 7/10 & 8/10 (1′ & 5′)
 BW: 1590 g HC: 29.5 cm Height: 45 cm
 DX: IUGR
The newborn was Hospitalized and managed
 BS was normal HB: 23.9
After 2 days bilirubin was 16 and phototherapy was started
CXR: normal blood culture: WNL
 After one Week the infant was discharged
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Intra Uterine Growth Retardation
 Intra Uterine Growth Restriction
 Small for gestational age (SGA)
 Foetal growth restriction
 'wasted' and 'stunted'
Please also see notes pages for more details in most of the slides
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Definition
 Intrauterine growth retardation (IUGR)
occurs when the unborn baby is at or below the
10th weight percentile for his or her age (in
weeks). The foetus is affected by a pathologic
restriction in its ability to grow.

Low birth weight (LBW) means a baby
with a birth weight of less than 2500Gms,
which could be due to IUGR or Prematurity
Please also see notes pages for more details in most of the slides
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Classification
Symmetricl
the baby's head and body
are proportionately small.
may occur when the
foetus experiences a
problem during early
development.
Asymmetrical
baby's brain is abnormally
large when compared to the
liver.
may occur when the foetus
experiences a problem
during later development
In a normal infant, the brain weighs about three times more than the liver. In
asymmetrical IUGR, the brain can weigh five or six times more than the liver.
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Classification
Newer Classification: 1. Normal small fetuses- have no structural abnormality,
normal umbilical artery & liquor but wt., is less.They are
not at risk and do not need any special care.
2. Abnormal small fetuses- have chromosomal anomalies
or structural malformations. They are lost cases and
deserve termination as nothing can be done.
3. Growth restricted fetuses- are due to impaired
placental function.Appropriate & timely treatment or
termination can improve prospects.
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Aetiology
 The foetal growth is dependent on multiple factors.
 IUGR resulting in SGA babies can result from many
factors known and unknown either acting alone or in
conjunction or in association .
 The aetiologic determinants of IUGR have two
measures of effect: relative risk and etiologic fraction.
 Most of the evidence on aetiologic determinants is
based on observational studies and systematic
overviews or meta-analyses of such studies.
 In a majority of cases (40%) the cause is unknown–
probably due to placental insufficiency (idiopathic).
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Aetiology
1. General- Racial / Ethnic origin, Small maternal /
paternal height / weight, Foetal sex.
2.
3.
4.
5.
Maternal causes.
Foetal causes.
Placental causes.
Idiopathic- In a majority of cases (40%) the
cause is unknown– probably due to placental
insufficiency.
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Maternal Risk Factors
 Has had a previous baby who suffered from
IUGR.
 Extremes of age.
 Is small in size (Ht & Wt).
 Has poor weight gain and malnutrition during
pregnancy.
 Is socially deprived.
 Uses substances (like tobacco, narcotics, alcohol)
that can cause abnormal development or birth
defects.
 Has a low total blood volume during early
pregnancy.
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Maternal Risk Factors

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

Is pregnant with more than one baby.
High altitude.
Drugs like anticoagulants, anticonvulsants.
Has a cardio-vascular disease-preeclampsia,
hypertension, cyanotic heart disease, cardiac
disease Gr III & IV, diabetic vascular lesions.
 Chronic kidney disease
 Chronic infection- UTI, Malaria, TB, genital
infections
 Has an antibody problem that can make
successful pregnancy difficult (antiphospholipid
antibody syndrome, SLE).
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Fetal Risk Factors
 Exposure to an infection-German measles (rubella),
cytomegalovirus, herpes simplex, tuberculosis, syphilis, or
toxoplasmosis, TB, Malaria, Parvo virus B19.
 A birth defect (cardiovascular, renal, anencephally,
limb defect, etc).
 A chromosome defect- trisomy-18 (Edwards’
syndrome),21(Down’s syndrome), 16, 13, xo (turner’s
syndrome.
 A primary disorder of bone or cartilage.
 A chronic lack of oxygen during development
(hypoxia).
 Developed outside of the uterus.
 Placenta or umbilical cord defects.
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Placental Factors
 Uteroplacental insufficiency resulting from -.
 Improper / inadequate trophoblastic invasion and
placentation in the first trimester.
 Lateral insertion of placenta.
 Reduced maternal blood flow to the placental bed.
 Foetoplacetal insufficiency due to-.
 Vascular anomalies of placenta and cord.
 Decreased placental functioning mass-.
» Small placenta, abruptio placenta, placenta previa, post
term pregnancy.
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Diagnosis
Intrauterine  IUGR can be difficult to diagnose.
 Presence of risk factors.
 Inadequate growth detected by serial
measurement of Wt., abdominal girth and
fundal Ht.
 Ultrasound to evaluate the foetal growth.
 Inadequate foetal growth.
 Reduced AFI.
 Placental calcification.
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Diagnosis
Neonatal  Low ponderal index (Wt./Fl).
 Decreased subcutaneous fat.
 Presence / appearance of –
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Hypoglycemia,
Hyperbilirubinemia,
Narcotizing enterocolitis,
Hyper viscosity syndrome
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Neonate and Placenta in IUGR
 Normal & IUGR Newborn
babies
 Normal & IUGR Placentas
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Prevention
 Strategies include
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prenatal care modalities,
protein/energy supplementation,
treatment of anaemia,
vitamin/mineral supplementation,
fish oil supplementation
prevention and treatment of
» hypertensive disorders,
» foetal compromise
» infection.
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Prevention
 Strong evidence of benefit only for the
following interventions:
 balanced protein/energy supplementation,
 strategies to reduce maternal smoking,
 antibiotic administration to prevent urinary tract
infections and
 antimalarial prophylaxis.
 Few statistically significant reductions in the
risk of IUGR have been demonstrated with
other interventions.
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Surveillance
 Unless delivery occurs, once treatment begins the
foetus must undergo surveillance.
 The purpose - to identify further progression of
the disease process that would jeopardize the
foetus to a point that it would be better to be
delivered than to remain in utero.
 There are four testing modalities which are helpful
-Non-Stress Test, Amniotic Fluid Index,
Doppler of the Umbilical Artery & Biophysical
Profile, each of which addresses different
aspects of surveillance.
 Combination of tests are better than an isolated
test.
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Surveillance

Non- Stress Test (NST)
This simplest to perform test should b used first in
the surveillance of IUGR foetuses. With the help of
a heart rate monitor, the changes in the foetal heart
rate with foetal movement are to be determined. If
the heart rate increases more than 15 beats for
more than 15 seconds, this is considered to be a
reactive test. If the heart rate does not accelerate,
remains flat, or decreases, then this is an abnormal
test. The problem with this test is that it changes
late in the course of the disease and is not an early
predictor of adverse outcome.
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Surveillance

Amniotic Fluid Index (AFI)
The vertical depth of four pockets of amniotic
fluid are measured by USG, to obtain a total
AFI. This method allows for comparison of
changes in amniotic fluid with time. In the
normal foetus the AFI remains relatively
constant. In the foetus with IUGR, it may
decrease slowly, or decrease abruptly with
time. A decrease in AFI may occur before
there are changes in the non-stress test.
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Surveillance

Amniotic Fluid Index (AFI)
The current
recommendations
are that if the AFI
decreases below 8
after 35 weeks,
then delivery
should occur.
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Surveillance

Doppler of the Umbilical Artery
When IUGR is
diagnosed, the value of
sequential studies of the
umbilical artery Doppler
waveform is to determine
if the Resistance Index is
increasing or decreasing.
If it is increasing, then
this signifies a
deteriorating condition.
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Surveillance

Biophysical Profile
 This test combines the NST and the AFI with
foetal movement, breathing, and muscle tone.
 If each of the tests are normal they are given a score
of 2. If abnormal, a score of 0.
 A score of 6 or less suggests the foetus is at risk for
adverse outcome.
 While the biophysical profile is an useful test,
when it becomes abnormal the foetus may have
already suffered some damage
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Treatment

IUGR has many causes, therefore, there is
not one treatment that always works.
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Treatment
 Although there are many causes of IUGR, the treatment
consists of either delivery or remaining in utero and
improving blood flow to the uterus.
 When blood flow is improved, the delivery of oxygen and
other nutrients to the foetus occurs. If the foetus is lacking
in these substances, their increased availability may result
in improved growth and development.
 If IUGR is caused by a problem with the placenta and the
baby is otherwise healthy, early diagnosis and treatment
of the problem may reduce the chance of a serious
outcome.
 There is no treatment that improves foetal growth, but
IUGR babies who are at or near term have the best
outcome if delivered promptly.
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Treatment
 Maternal bed rest
This is the initial approach for the treatment
of IUGR. The benefit of bed rest is that it
results in increased blood flow to the uterus.
Studies have shown, however, that in most
cases bed rest at home is just as effective
as bed rest in the hospital environment.
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Treatment
 Maternal bed rest
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Treatment
 Aspirin Therapy
 The use of aspirin to treat foetuses with IUGR is
still controversial.
 If aspirin is used, it may be advantageous if
given to patients before 20 weeks of gestation.
It is minimal to limited benefit if given at the time
of diagnosis (third trimester).
 At the present time it is not recommended as a
form of prevention for low risk patients.
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Treatment
 Other Forms of Treatment
 Other forms of treatment that have been
studied are nutritional supplementation, zinc
supplementation, fish oil, hormones and
oxygen therapy.
 Limited studies are available regarding the use
of these modalities in the treatment of IUGR.
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Treatment
Judge Optimum Time Of Delivery
RISK OF PREMATURITY
 DIFFICULT EXTRA
UTERINE
EXISTENCE
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RISK OF IUD
 HOSTILE INTRA
UTERINE
ENVIRONMENT
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Short Term Risks of IUGR
 Increased perinatal morbidity and mortality.
 Intra uterine / Intrapartum death.
 Intrapartuum foetal acidosis characterized by-.
»
»
»
»
Late deceleration.
Severe variable deceleration.
Beat to beat variability.
Episodes of bradicardia.
 Intrapartum foetal acidosis may occur in as many as
40 % of IUGR, leading to a high incidence of LSCS.
 IUGR infants are at greater risk of dying because of
neonatal complications- asphyxia, acidosis, meconium
aspiration syndrome, infection, hypoglycemia, hypothermia,
sudden infant death syndrome.
 IUGR infants are likely to be susceptible to infections
because of impaired immunity
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Long term Prognosis
 Babies who suffer from IUGR are at an increased risk for
death, low blood sugar, low body temperature, and
abnormal development of the nervous system. These risks
increase with the severity of the growth restriction.
 The growth that occurs after birth cannot be predicted with
certainty based on the size of the baby when it is born.
 Infants with asymmetrical IUGR are more likely to catch
up in growth after birth than are infants who suffer from
prolonged symmetrical IUGR.
 If IUGR is related to a disease or a genetic defect, the
future of the infant is related to the severity and the nature
of that disorder.
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Long term Prognosis
 IUGR infants are more likely to remain small than those of
normal birth weight. They will need the special attention of
primary health, nutrition and social services during infancy
and early childhood.
 Implication of IUGR can be life long affecting:
 Body size growth, composition and physical
performance.
 Immunocompetence.
 It appears to predispose to adult adult-onset, degenerative
diseases like maturity onset diabetes and cardiovascular
diseases.
 Each case is unique. Can not reliably predict an infant's
future progress.
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syndrome
 “mekonionarion” – “opium like” (Aristotle)
 Meconium stained amniotic fluid – 8-15 % of all
deliveries.
 5% of them – meconium aspiration syndrome
 5% mortality
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Origin and composition
 Meconium is recognized – 70-85 d of gestation
 Composition:
» Water, Mucopolysaccharides, Cholesterol and sterol precursos,
Protein, Lipid, Bile acids and salts, Enzymes, Blood group
substances, Squamous cell, Vernix caseosa
 No bacteria!
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In utero passage
 Risk factors associated with in utero passage of meconium:
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Postterm pregnancy
Little/no amniotic fluid at amniotomy
Oligohydramnion by US
IUGR/ placental insufficiency
Maternal HTN
Preeclampsia
Maternal drug abuse (tobacco, cocaine).
 Gestational age > 34w – increasingly present with advancing
gestational age.
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Pathophysiology
 As the GI tract matures:
vagal stimulation  peristalsis+ rectal sphincter
relaxation  meconium
 Etiology not well understood:
 Fetal response to intra-uterine stress: hypoxia 
increased vagal tone
 Transient compression of umbilical cord/head 
increased vagal tone
 Maturation of of fetal intestinal function
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Timing of the initial insult:
 Traditional belief: immediately after birth
 Several investigations: Most cases occur in
utero when fetal gasping is initiated before
delivery.
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Effects of meconium:
 Reduce antibacterial activity (perinatal bacterial
infection)
 Irritating to fetal skin ( erythema toxicum)
 The most severe complication of meconium
passage in utrro is aspiration of stained amniotic
fluid before, during, and after birth
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Meconium aspiration syndrome pathophysiology
 Airway obstruction:
 Chemical pneumonitis:
 Surfactant dysfunction:
 Umbilical vessel damage
 Persistent pulmonary hypertension of the
newborn
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Airway obstruction:
 Immediate : obstruction of large airways: (volume
dependent ):
hypoventilation => hypoxemia, hypercapnea, acidosis
 Central clearing – obstruction of small airways:
 Complete  athelectasis
 Partial  air trapping (ball valve phenomenon)  hyperdistention of
alveoli  increaesed lung resistance during exhalation
 pneumothorax, pneumomediastinum , pneumopericardium.
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Chemical pneummonitis:
 50% of cases
 Enzemes, bile salts, fats – irritants PMN, MQ,
inflammatory mediators.
 Chemical pneumonitis, edema (6h)  inflamation
(24h)
 Hyalin membranes, hemorrhage, vascular necrosis can
occur.
 Bacterial superinfection.
 Activated Vasoactive mediators play a role in the
develipment of PPHN.
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Chemical pneummonitis:
 50% of cases
 Enzemes, bile salts, fats – irritants PMN, MQ,
inflammatory mediators.
 Chemical pneumonitis, edema (6h)  inflamation
(24h)
 Hyalin membranes, hemorrhage, vascular necrosis can
occur.
 Bacterial superinfection.
 Activated Vasoactive mediators play a role in the
develipment of PPHN.
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Surfactant dysfunction
 Free fatty acids (paimitic, stearic, oleic) –
higher minimal surface tention than surfactant
(striping effect)
 decreased lung compliance
 concentration dependent
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Umbilical vessel damage
 Umbilical vessels exposed to meconium  may
cause severe focal inflammation injury.
 Spasm and necrosis  fetal hypoperfusion
 1% meconium induced umbilical vascular
necrosis among meconium stained placentas.
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Persistent pulmonary hypertension of
the newborn
 Final common pathway for the severe morbidity and
mortality in infants with MAS.
 Hypoxia  Pulmonary arterial vasoconstriction.
 Abnormal pulmonary arterial muscularization  m/p chronic change
 Association between MAS and PPHN :
 Direct pathogenic cause of lung damage
 Simple marker of chronic intrauterine hypoxia
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Risk factors of MAS developing into
PPHN
 “Risk factors of meconium aspiration syndrome
developing into persistent pulmonary
hypertension of newborn.
Acta Paediatr Taiwan. 2004 Jul-Aug;45(4):2037” – 362 cases of MAS (17% with PPHN).
 Pneumothorax, change in FHR base line,
asphyxia  most important risk factors
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Risk and severety of MAS:
 Degree of contamination of the amniotic fluid and Presence
of meconium in the airway at delivery  is meconium itself a
direct primary cause of morbidity mortality?
 MAS is commonly associated with chronic hypoxia is
meconium a marker of fetal maturation of chronic fetal
hypoxia?
 Asphyxia, pneumothorax, PPHN – the most important risk
factors of mortality in MAS.
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Clinical presentation:

Depressed at birth

Early onset of respiratory distress (within 2 h)
» Mild tachypnea
» cyanosis
» Dyspnea: granting, ala nazi, intercostal retraction
» Barral chest (presence of air trapping)
» respiratory failure

Auscultayion: “wet” inspiratory crackles, occasional expiratory noises

Severe Mas:
» Hypoxemia – RL shant
» Persistant fetal circulation
» PPHN – hypoxic pulmonary arterial vasoconstriction – acidosis, hypercapnea,
hypoxemia (prenatal & perinatal maladaptation)
» Cardiopulmonary failure
» acidosis
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Complication:
 PPHN
 AIR LEAK
 PULMONARY HEMORRAGE
 ASPHYXIA COMPLICATIONS
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Laboratory:
 Hypoxemia (RL shunt)
 Hypercarbia (in significant obstruction)
 Respiratory alkalosis (hyperventilation)
 Combined respiratory and metabolic acidosis
(severe disease – respiratory failure)
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Chest x-ray
 73% - positive x-ray findings
 Global atelectasis – early
 Patchy dense opacifications (decreased vantilation)
accompanied by areas of hyperinflation
 Widespread infiltrates
 Consolidations
 Small pleural effusion (30%)
 Pneumothorax/ pneumomediastinum (25%)
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Prenatal diagnosis and prevention:
 Diagnosis of fetus “at risk” – monitoring fetal
status.
 Thick VS thin meconium
 Meconium and FHR abnormalities
 Amnioinfusion during labor
 Nasopharyngeal suctioning
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Upon delivery intervention:
 “combined approach” : nasopharengeal suctioning +
neonatal trachea suction.
 Thick meconium + depressed infant  tracheal suction
- marked reduction in morbidity and mortality.
 The American Academy of pediatrics Neonatal
Resuscitation Program Steering Guidelines
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management
 Minimize agitation (prevent additional acidosis and
hypoxemia) – optimal thermal environment, minimal
handling, muscle relaxation.
 NGT
 Respiratory care
 Maintain systemic blood pressure (RL shunt)
 Antibiotics.
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
MAS treatment – ventilation
Main target: oxigenation! – PaO2
60-90mmHg
support:

difficulty with oxigenation positive airway pressure (CPAP) – improves
ventilation, stabilizes small airways.

Respiratory acidosis/severe respiratory distress  mechanical ventilation – sPO2> 50
mm Hg with FiO2 – 100% & pH< 7.2 . sedation! Relaxation!

Surfactant

iNO

failed conventional ventilation – HFJV, HFO

ECMO
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SURFACTANT
 Lung lavage using sufractant in MAS is currently being investigated
“Treatment of severe meconium aspiration syndrome with porcine
surfactant: a multicentre, randomized, controlled trial”
Acta Paediatr. 2005 Jul;94(7):896-902.
“ Pulmonary function after surfactant lung lavage followed by surfactant
administration in infants with severe meconium aspiration syndrome”.
J Matern Fetal Neonatal Med. 2004 Aug;16(2):125-30.
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Steroids
 Pathophysiology: anti-infalammatory properties.
 Corticosteroid treatment, started early, show some
improvement in oxigenation and pulmonary
hemodynamics durind acute phase.
 Effect on morbidity and mortality  Cochrane
Database Syst Rev, 2003  insufficient evidence.
 Further research: clinucal significant, optimal timing,
dosing.
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!!!‫תי‬
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Case 2
25 Y G1 42 W Single
CC: LP
PNC: (-)
PMH: opiate abuser
FH: Term V/E: 3 – 4 cm & me conium stained Amniotic
fluid
The new born birthed by C/S
The vernix , umbilical cord and nails was me conium –
stained endoteracheal suction was performed
The new born had respiratory distress with marked tachypnea
and cyanosis .
APGAR: 3/10 & 6/10 (1′ & 5′)
Auscultation reveals rales
The new born was hospitalized in NICU
Because of Eyes Discharged Gentamicin and cefotaxim was
started
After 6 days the infant was discharged
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