INTRA UTERINE GROWTH RETARDATION - NURSING ASSIGNMENT

INTRODUCTION

        Expert care of new born babies requires an understanding of intrauterine growth patterns and they relate to gestational age. Anderson and Hay (1999) define IUGR as a rate of fetal growth that is less than normal for the population and for the growth potential of a specific baby.

DEFINITION

        Intra uterine growth restriction is said to be present in those babies whose birth weight is below the tenth percentile of the average for the gestational age.

INCIDENCE

·        Dysmaturity comprises about one third of low birth weight babies

·        In developed countries its overall incidence is about 2-8%

·        The incidence among the term babies is about 5% and that among the post term babies is about 15%

NOMENCLATURE

·        SGA and IUGR are too often used synonymously although there is a degree of overlap.

·        SGA fetus is not necessarily growth retarded

·        The baby may be constitutionally small

·        Similarly late onset of pathological cessation of growth may produce a baby with typical features of IUGR, but may not be small for gestation (i.e, appropriate for gestational age)

·        However, both attempt to identify fetuses or neonates that are small for reasons other than being preterm

·        Normal fetal growth is characterized by cellular hyperplasia followed by hyperplasia and hypertrophy and lastly by hypertrophy alone

TYPES

·        Fetuses that are small and healthy. The birth weight is less than 10^th percentile for their gestational age. The have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course

·        Fetuses where growth is restricted by pathological process (true IUGR). Depending upon the relative size of their head, abdomen, and femur the fetuses are subdivided into

Ø     Symmetrical or Type I

Ø     Asymmetrical or Type II

Symmetrical (20 percent)

·        The fetus is affected from the noxious effect very early in the phase of cellular hyperplasia

·        The total cell number is less

·        This form of growth retardation is most often caused by structural or chromosomal abnormalities or congenital infection (TORCH)

·        The pathologic process is intrinsic to the fetus and involves all the organs including the head.

Asymmetrical (80 percent)

·        The fetus is affected in later months during the phase of cellular hypertrophy

·        The total cell number remains the same but size is smaller than normal

·        The pathologic process that too often result in asymmetric growth retardation are maternal diseases extrinsic to the fetus

·        These disease after the fetal size by reducing uteroplacental blood flow or by restricting the oxygen and nutrient transfer or by reducing placental size

Features of Symmetrical and Asymmetrical IUGR Fetuses

Uniformly small	Head larger than abdomen
Ponderal index – normal	Low
Head: Abdomen Femur: Abdomen ratios normal	Elevated
Etiology: Genetic disease or infection (intrinsic to fetus0	Chronic placental insufficiency (Extrinsic to Fetus)
Total cell number – less Cell size – normal	Normal Smaller
Neonatal course – complicated with poor prognosis	Usually uncomplicated having good prognosis

ETIOLOGY

        The causes of fetal growth retardation can be divided into four groups

·        Maternal

·        Fetal

·        Placental

·        Unknown

Maternal

·        Constitutional – some women, maternal genetic and racial factor may be associated with small babies and is not necessarily and undesirable event

·        Maternal nutrition before and during pregnancy critical substrate requirement for the fetus such as glucose, aminoacids and oxygen are lacking during pregnancy

·        This is an important causes of small weight of the babies in developing countries

·        As most of the fetal weight gain (two-thirds) occur beyond 24^th week of pregnancy, malnutrition, anemia, hypertension, antiphospholipid syndrome in the second half of pregnancy play significant role in reduction of the birth weight

·        Poor weight gain during pregnancy

·        Low blood oxygen as in cyanotic heart disease

·        Inadequate substrate level – malaborption syndrome

·        Toxins – Alcohol, smoking, chronic renal failure chronic urinary tract infection etc

Fetal

        There is enough substrate in the maternal blood and also crosses the placenta is not utilized by the fetus. The failure of nonutilization may be due to:

·        Congential anomalies either cardiovascular, renal or others

·        Chromosomal abnormality is associated with 8-12% of growth retarded infants. The common abnormalities aretaisomy 21, trisomy 18 (Edwards syndrome), trisomy 16, trisomy 13, and turners syndrome.

·        Accelerated fetal metabolism due to TORCH agents (toxo pla sosis, rubella, cytomegalovirus and herpes simplex) and parvo virus B 19.

·        Multiple pregnancy- There is mechanical hindrance growth and excessive fetal demand.

Placental

        The causes include cases of poor uterine blood flow to placental site for a long time. This leads to chronic placental insufficiency with adequate substrate transfer.

·        This occurs in conditions such as preeclampsia, essential hypertension, chronic nephritis, organic heart disease, placental and cord abnormalities such as chronic placental abruption, infarction, small placenta, circumvallate placneta, vellamentous insertion of cord etc

·        Unknown: The cause remains unknown in about 40 percent

DIAGNOSIS

Clinical

·        Clinical palpation

·        Symphysis fundal height

·        Maternal weight gain

·        Measurement of the abdominal girth

Biophysical

·        Head circumference

·        Femur length

·        Aminotic fluid volume

·        Doppler velocimetry

·        To exclude fetal structural abnormalities by sonographic evaluation

·        Ponderlal index (PI)

COMPLICATIONS

Fetal

·        Antenatal : Chronic fetal distress, fetal death

·        Intranatal: Hypoxia and acidosis

·        After birth

Immediate

·        Asphyxia (intrauterine and neonata)

·        Hypoglycemia due to shortage of glycogen reserve in the liver as a result of chronic hypoxia

·        Meconium aspiration pneumonia

·        Microcoagulation leading to DIC during first day of life

·        Hypothermia

·        Pulmonary haemorrhage

·        Polycythaemia

·        Hyperviscosity syndrome

·        Necrotizing enterocolitis due to reduced intestinal blood flow

Late

·        Symmetrical growth retarded baby is likely to grow slowly after birth

·        Whereas the asymmetrical one is more likely to grow faster after birth

·        The fetuses having retardation of growth evidence before third trimester are likely to have retarded neurologic and intellectual development in infancy

·        The worst prognosis is for IUGR caused by congenital infection congenital abnormalities and chromosomal defects

Maternal

·        Per se fetal growth retardation does not cause any harm to mother

·        The disease process like pre-eclampsia, heart disease, malnutrition may be life threatening

·        Woman with a growth retarded infant, risk of having another is two fold

Mortality

·        The immediate neonatal mortality is about 6 times more than the normal new born or even similar weight appropriate to the shorter gestational age

·        Most of the babies die with 24 hours

·        The morbidity rate rises to about 50%

MANAGEMENT

General

·        At present there is no proven therapy for reversing growth retardation once it is established

·        Adequate bed rest specially in left lateral position

·        To correct malnutrition by balanced diet: 800 extra calories per day are to be taken

·        To institute appropriate therapy for the associated complicating factors likely to produce growth restriction

·        Avoidance of smoking and alcohol

·        Maternal hyperxoygenation (55%) for short term prolongation of pregnancy

·        Low dose aspirin (50mg daily) may be helpful in very selected cases with history of recurrence

Termination of Pregnancy

·        Presence of fetal abnormality

·        Duration of pregnancy

·        Degree of growth restriction

·        Associated complicating factor

·        Degree of fetal compromise

·        Previous obstetric history

·        Facilities available at the place of delivery

Beyond 37 weeks

        Termination of pregnancy should be done

Before 37 weeks

        Uncomplicated mild IUGR, fortunately, the majority falls in this groups.

·        Usual treatment as outlined above to improve the placental function may be employed

·        The condition may be reversed and in such cases, the pregnancy is allowed to continue but the tendency to over run the expected date is to be curtailed by termination

Severe Degree of IUGR

·        If the lung maturation is achieved as evidence  phosphatidyl glycerol and L:S ratio of at least 2 from the amniotic fluid (aminocentesis) termination is done

·        If the lung maturation has not yet been achieved (premature lung maturation usually occurs in IUGR) one has to face dual problem

·        One of prematurity and other of growth restriction

·        These cases are few and far between and by the time severe growth restriction occurs, the baby attains a fair chance of survival ex-utero

·        The right time termination can be determined dexamethas one therapy is given to accelerate pulmonary maturation when gestational age is less that 36  weeks

·        Cordicosteroids reduce the risk of neonatal HMD and intraventricular haemorrhage (IVH)

NURSES ROLE

        The most important single factor is high standard of nursing and one trained nurse can adequate measures to rectify the defect can be life saving in many an occasion.

·        The temperature should be taken twice daily and the baby should be weighted daily to know whether over or in dehydrated

·        Constant supervision specially during the crucial first 48 hours is imperative

·        Mother should be allowed to her baby in the nursery

·        Mother is thought for the general care of baby and manual expression of breast feeding milk by pressing over the Gerola and nipple

·        Intelligent observation, prompt recognition of the abnormality and adequate measure to rectify the defect can be life saving in many an occasion.

CONCLUSION

        Anderson and Hay define IUGR as a rate of fetal growth that is less than normal for the population and for the growth potential of a specific baby.

        The causes are maternal, placental and fetal factors are represent a mix of genetic mechanisms and environmental influences through which growth potential is expressed.

BIBLIOGRAPHY

·        A Text Book of Obstetrics, D.C.Dutta

5^th Edition, 2011, Page No.496-501

·        A Text Book of Midwives, Gillian Fletcher

14^th Edition, 2003, Page No.782-784