Intensive Care Nursery House Staff Manual

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Intensive Care Nursery House Staff Manual
69
Copyright © 2004 The Regents of the University of California

Intrauterine Growth Retardation
CLINICAL SIGNIFICANCE: Intrauterine growth retardation (IUGR) affects 3-10% of pregnancies; 20% of stillborn infants have IUGR. Perinatal mortality rates are 4-8 times higher for growth retarded infants, and morbidity is present in 50% of surviving infants. DEFINITIONS and CLASSIFICATION: -AGA, appropriate for gestational age: Birth weight is between 10th and 90th percentile for infant’s gestational age (GA). -LGA, large for gestational age: Birth weight >90th percentile for GA. - SGA, small for gestational age: Birth weight <10th percentile for GA. Other definitions are sometimes used for SGA, including <3rd percentile for GA or more than 2 S.D. below the mean. -IUGR vs. SGA: IUGR refers to deviation and reduction in expected fetal growth pattern. Multiple adverse conditions inhibit normal fetal growth potential. Not all IUGR infants are SGA. ASYMMETRIC vs. SYMMETRIC GROWTH RETARDATION: Most growth retarded infants have asymmetric growth restriction. First there is restriction of weight and then length, with a relative “head sparing” effect. This asymmetric growth is more commonly due to extrinsic influences that affect the fetus later in gestation, such as preeclampsia, chronic hypertension, and uterine anomalies. Postnatal growth after IUGR depends on cause of growth retardation, postnatal nutritional intake, and social environment. Symmetric growth retardation affects all growth parameters. In the human brain, most neurons develop prior to the 18th week of gestation. Early gestational growth retardation would be expected to affect the fetus in a symmetric manner, and thus have permanent neurologic consequences for the infant. Examples of etiologies for symmetric growth retardation include genetic or chromosomal causes, early gestational intrauterine infections (TORCH) and maternal alcohol use. CAUSAL FACTORS: A. Maternal -Before pregnancy: • Prepregnancy weight influences fetal size • Periconceptual nutritional status can affect embryogenesis (e.g., folate deficiency). -During pregnancy: Factors that may adversely affect fetal growth include: • Low pre-pregnancy weight and small maternal size • Recent pregnancy and/or high parity • Poor weight gain during pregnancy, especially in latter half • Chronic illness - such as malabsorption, diabetes, renal disease • Inadequate or poorly balanced intake associated with alcoholism, drug abuse, poverty, adolescence, anorexia nervosa, food faddism • Maternal drug and alcohol use also influence maternal nutrition. • Decreased O2 availability to fetus (e.g., high altitude, severe maternal anemia) Intrauterine Growth Retardation
70
Copyright © 2004 The Regents of the University of California

B. Uterine and placental factors that can adversely affect fetal growth include inadequate placental growth, uterine malformations, decreased utero-placental blood

flow (e.g., toxemias of pregnancy, diabetic vasculopathy) and multiple gestations C. Fetal causes are unusual, include familial genetic and chromosomal abnormalities and intrauterine infections (i.e., TORCH), and usually have a poor long term prognosis. PATHOPHYSIOLOGY: With maternal or placental causes of IUGR, there is decreased placental transfer of nutrient (including oxygen) resulting in reduced fetal body stores of lipids and glycogen resulting in neonatal hypoglycemia; chronic hypoxemia stimulates erythropoietin production leading to polycythemia. These infants are also at increased risk for perinatal asphyxia. Other associated problems include hypocalcemia, pulmonary hemorrhage, hypothermia and, with IUGR associated with toxemia, thrombocytopenia and leukopenia. With fetal causes, decreased growth is constitutive (due to genetic factors) or secondary to infection. ASSESSMENT and MANAGEMENT: -Treat asphyxia if present. -Measure weight, head circumference and length to categorize the type of IUGR. -Careful physical examination for anomalies and dysmorphic features. -Blood glucose and hematocrit to detect hypoglycemia and polycythemia. See sections on Hypoglycemia (P. 153) and on Polycythemia (P. 112). -Serum Ca++, WBC count with differential and platelet count. -Infants with IUGR due to placental factors have ↑ O2 consumption. This ↑ insensible water loss to a variable degree (as much as 20-30%). Compensate for this by increasing IV fluid intake. These infants may also need greater intake (>150 mL/kg/d and >100 kcal/kg/d) to achieve adequate growth. -Further workup and treatment depends on abnormalities identified on history and physical examination. OUTCOME: -Perinatal mortality for IUGR infants is 5-20 times greater than for AGA, mainly due to intrauterine death, perinatal asphyxia, and congenital anomalies. -Neurologic morbidity is 5-10 times higher than for AGA infants, especially for infants with ↓ head circumference at birth. Intellectual and motor function (excluding those with congenital infections, chromosomal abnormalities) depends on adverse perinatal events and on the specific cause of growth restriction. Early identification and treatment of hypoglycemia and polycythemia improves outcome. Neurologic abnormalities are usual with genetic and infectious causes of IUGR. -Retarded growth: With placental causes of IUGR, catch-up growth occurs after birth, but these patients usually remain smaller than expected. -Fetal “programming” of cardiovascular disease: Recent studies implicate IUGR with adult onset of hypertension, coronary heart disease, hypercholesterolemia, and diabetes. These studies suggest that IUGR has long term affects on endocrine development and homeostasis.

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Small for gestational age
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Small for gestational age
Classification and external resources ICD-10 ICD-9 DiseasesDB MeSH P05., P07. 764, 765 31952 D007230

Small for gestational age (SGA) babies are those whose birth weight lies below the 10th percentile for that gestational age. Appropriate for gestational age (AGA) are those whose birth weight lies above the 10th percentile for that gestational age and below the 90th percentile for that gestational age.

Small for gestational age babies have usually been the subject of intrauterine growth restriction (IUGR), formerly known as intrauterine growth retardation.[1]

Gestational age and birth weight of infants born at 24 to 46 weeks' gestation. Infants are classified as large for gestational age (LGA), appropriate for gestational age (AGA), or small for gestational age (SGA). Another classification which takes in consideration only the weight and not the gestational age, is low body weight (LBW), VLBW and ELBW. Low birth weight (LBW) is defined as a fetus that weighs less than 2500 g (5 lb 8 oz) regardless of gestational age. Other definitions include Very Low Birth Weight (VLBW) which is less than 1500 g, and Extremely Low Birth Weight (ELBW) which is less than 1000 g.[2] Normal Weight at term delivery is 2500 g - 4200 g. SGA is not a synonym of LBW, VLBW or ELBW. Example: 35 week gestational age delivery, 2250g weight is appropriate for gestational age but is LBW. One third of low-birth-weight neonates-infants weighing less than 2500g - are small for gesational age. There is a 8.1% incidence of low birth weight in developed countries, and 6–30% in developing countries. Much of this can be attributed to the health of the mother during pregnancy. One third of babies born with a low birth weight are also small for gestational age.

Contents
[hide]
• • •

1 Diagnosis 2 Predetermining factors 3 Categories of growth restriction
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3.1 Symmetrical 3.2 Asymmetrical



4 Treatment

• •

5 Support 6 References

[edit] Diagnosis
The condition is generally diagnosed by measuring the mother's uterus, with the fundal height being less than it should be for that stage of the pregnancy. If it is suspected, the mother will usually be sent for an ultrasound to confirm.

[edit] Predetermining factors
The risk factor/etiology can be broadly divided into 3 categories• • • Fetal Maternal Placental

The primary risk factor is that development of the placenta is insufficient to meet the demands of the fetus, resulting in malnutrition of the developing fetus. There are numerous contributing factors, of both environmental and genetic origin:
• • •

Environmental factors such as poor nutrition, tobacco smoking, drug addiction or alcoholism Severe anaemia (although hydrops may also occur) Thrombophilia (tendency for thrombosis) Prolonged pregnancy Pre-eclampsia Chromosomal abnormalities Damaged or reduced placental tissue due to:
○ ○ ○


• •



Chronic renal failure Sickle cell anemia Phenylketonuria

• •

Infections such as rubella, cytomegalovirus, toxoplasmosis or syphilis Twins and multiple births.

[edit] Categories of growth restriction
There are two distinct categories of growth restriction, indicating the stage at which the development was slowed. Small for gestational age babies can be classified as having symmetrical or asymmetrical [asymmetrical] growth restriction.[3][4]

[edit] Symmetrical
Symmetrical growth restriction, less commonly known as global growth restriction, indicates that the fetus has developed slowly throughout the duration of the pregnancy and was thus affected from a very early stage. The head circumference of such a newborn is in proportion to the rest of the body. Common causes include:

• •

Early intrauterine infections, such as cytomegalovirus, rubella or toxoplasmosis Chromosomal abnormalities Chronic high blood pressure Severe malnutrition Anemia Maternal substance abuse (prenatal alcohol use can result in Fetal alcohol syndrome)

• • •


[edit] Asymmetrical
Asymmetrical growth restriction occurs when the embryo/fetus has grown normally for the first two trimesters but encounters difficulties in the third, usually pre-eclampsia. Such babies have a disparity in their length and head circumference when compared to the birth weight. A lack of subcutaneous fat leads to a thin and small body out of proportion with the head. Other symptoms include dry, peeling skin and an overly-thin umbilical cord, and the baby is at increased risk of hypoxia and hypoglycaemia.

[edit] Treatment
Possible treatments include the early induction of labour, though this is only done if the condition has been diagnosed and seen as a risk to the health of the fetus.

[edit] Support
The MAGIC Foundation for Children's Growth[1]

[edit] References
1. ^ "eMedicine - Intrauterine Growth Retardation : Article by Vikram S Dogra, MD". http://www.emedicine.com/radio/topic364.htm. Retrieved 2007-11-28. 2. ^ "eMedicine - Extremely Low Birth Weight Infant : Article by KN Siva Subramanian, MD". http://www.emedicine.com/ped/topic2784.htm. Retrieved 2007-11-28. 3. ^ "Intrauterine Growth Restriction". http://www.obgyn.ufl.edu/ultrasound/MedinfoVersion/sec7/7_3.html. Retrieved 2007-11-28. 4. ^ "Intrauterine Growth Restriction: Identification and Management - August 1998 - American Academy of Family Physicians". http://www.aafp.org/afp/980800ap/peleg.html. Retrieved 200711-28.

[hide]
v•d•e

Certain conditions originating in the perinatal period / fetal disease (P, 760779)
placenta: Placenta praevia · Placental insufficiency · Twin-toMaternal factors and twin transfusion syndrome complications of pregnancy, chorion/amnion: Chorioamnionitis labour and delivery umbilical cord: Umbilical cord prolapse · Nuchal cord · Single umbilical artery

Length of gestation Small for gestational age/Large for gestational age · Preterm and fetal growth birth/Postmature birth Birth trauma Cephalhematoma · Brachial plexus lesion (Erb's palsy, Klumpke paralysis) Intrauterine hypoxia · Infant respiratory distress syndrome · Transient tachypnea of the newborn · Meconium aspiration Respiratorysyndrome · pleural disease (Pneumothorax, Pneumomediastinum) · WilsonMikity syndrome · Bronchopulmonary dysplasia Pneumopericardium · Persistent fetal Cardiovascular circulation Vitamin K deficiency (Haemorrhagic disease of the newborn) · Hemolytic disease of the newborn (ABO HDN • Anti-Kell Haemorrhagic and HDN • Rhesus c HDN • Rhesus D haematological/ HDN • Rhesus E HDN) · Rh hematologic disease disease · Hydrops fetalis · Hyperbilirubinemia (Kernicterus, Neonatal jaundice) Velamentous cord insertion Ileus · Necrotizing enterocolitis · Digestive system Meconium peritonitis Integument and Erythema toxicum temperature regulation Nervous systemPeriventricular leukomalacia Gray baby syndrome · muscle tone Musculoskeletal (Congenital hypertonia, Congenital system hypotonia) Perinatal infection (Congenital rubella syndrome, Neonatal herpes simplex) · Omphalitis · Neonatal sepsis (Group B Other disorders streptococcal infection) Stillbirth/Perinatal mortality

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obstetric navs: pregnancy, conditions of mother/fetus/maternal transmission, eponymous signs, proc Retrieved from "http://en.wikipedia.org/wiki/Small_for_gestational_age" Categories: Obstetrics | Pediatrics
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AIIMS- NICU protocols 2007

Management of infants with intra-uterine growth restriction
Ashok K Deorari, Ramesh Agarwal , Vinod K Paul Division of Neonatology, Department of Pediatrics All India Institute of Medical Sciences Ansari Nagar, New Delhi –110029 Address for correspondence: Dr Ashok Deorari Professor Department of Pediatrics All India Institute of Medical Sciences Ansari Nagar, New Delhi 110029 Email: [email protected] Downloaded from www.newbornwhocc.org 1 AIIMS- NICU protocols 2007 Abstract Intra-uterine growth restriction (IUGR) contributes to almost two-thirds of LBW infants born in India. Poor nutritional status and frequent pregnancies are common predisposing conditions in addition to obstetric and medical problems during pregnancy. Growth restriction may be

symmetrical or asymmetrical depending on the time of insult during pregnancy. The pathological insult in an asymmetrical IUGR occurs during the later part of the pregnancy and has a brainsparing effect. Common morbidities are more frequent in <3rd percentile group as compared to 3rd– 10th percentile group. Guidelines for management of IUGR neonates in these two groups have been provided in the protocol. Downloaded from www.newbornwhocc.org 2 AIIMS- NICU protocols 2007 Introduction Nearly one third of neonates born in India are low birth weight (LBW), weighing less than 2500 grams at birth. A baby’s low birth weight is either the result of preterm birth (before 37 completed weeks of gestation) or due to intrauterine growth restriction (IUGR). Later condition is akin to malnutrition and may be present in both term and preterm infants. Neonates affected by IUGR are usually undernourished, undersized and therefore, low birth weight. Twothird LBW neonates born in India fall in this category1. Since IUGR neonates are more likely to suffer complications including cold stress and hypoglycemia, it is important that these infants are identified and managed appropriately at birth2. Even after recovering from neonatal complications, they remain more prone to poor physical growth, poor neurodevelopmental outcome, recurrent infection and chronic diseases (hypertension, hyperlipidemia, diabetes mellitus, coronary heart disease) later in life3. IUGR and SGA (Small-for-gestational age) Although both the terms are used inter-changeably and both denote malnutrition, there is a minor difference in the terminology. SGA a statistical definition, is used for neonates whose birth weight is lower than (less than 10th percentile for that particular gestational age) population norms. IUGR is a clinical definition and includes neonates with clinical evidence of malnutrition. This may be in the form of loose skin folds on the face and in the gluteal region, absence of subcutaneous fat and peeling of skin. Although most IUGR infants would also be SGA, it is possible that a small

minority of IUGR infants may have birth weights above the 10th percentile. These morphological IUGR infants would behave like SGA infants and should be managed along the same lines as SGA infants. For purposes of discussion in this paper, the term IUGR would include both the groups of infants . Downloaded from www.newbornwhocc.org 3 AIIMS- NICU protocols 2007 Etiology Poor nutritional status of the mother and frequent pregnancies are the major cause of IUGR. Mothers with a weight of less than 40 kg and a height of less than 145 cm often give birth to SGA infants. Insufficient nutritional intake during pregnancy also has an adverse effect on fetal weight. Maternal hypertension, pre-eclampsia, post-maturity, frequent pregnancies, multiple pregnancy, anemia, malaria and tobacco use are other causes of IUGR4-6. Chronic maternal diseases of heart, kidneys, lungs or liver may also lead to IUGR. Types of IUGR Infants with IUGR are often classified as having symmetrical (head circumference, length and weight equally affected) or asymmetrical (with relative head growth sparing) growth restriction. Infants with symmetric IUGR often have an earlier onset and are associated with causes that affect total fetal cell number including chromosomal, genetic, teratogenic, intrauterine infections and severe hypertensive etiologies. Asymmetric IUGR is often of a later onset, demonstrates preservation of blood flow to brain and is associated with poor maternal nutrition or late onset exacerbation of maternal vascular disease (pre-eclampsia, chronic hypertension)7. Clinical features IUGR or SGA infants are often term or near-term in gestation. Their birth weight usually falls below the 10th percentile8 The neonate has an emaciated look and loose skin because of lack of subcutaneous tissue. These are particularly prominent over the buttocks and the thighs. They look alert and are often plethoric. Comparison of the head circumference with chest circumference is

helpful in the identification of a SGA infant. In infants with appropriate growth, the head size is usually bigger than the chest by about 2-cm. In SGA infants, the head circumference usually Downloaded from www.newbornwhocc.org 4 AIIMS- NICU protocols 2007 exceeds the chest circumference by more than 3 cm. A preterm SGA infant would have a combination of clinical features suggestive of both, prematurity and IUGR9. Problems of SGA infants Common neonatal morbidities encountered in SGA infants born in our hospital are given in Table 1. The common morbidities encountered in IUGR neonates include: (a) perinatal asphyxia, (b) hypothermia, (c) hypoglycemia and (d) polycythemia. These morbidities are commoner in the more severely gr owth restricted babies (<3rd percentile) as compared to babies in the 3rd to 10th percentile category. From August 2004 to July 2005, 144 SGA babies were born in our hospital. 24 (17%) developed hypoglycemia and 14 (10%) had polycythemia requiring partial exchange transfusion. Amongst 24 babies with hypoglycemia 50% of the total episodes occurred at 2 h, 22% at 48 h, 11% each at 6 and 12 h and only 4% each at 24 and 72 h of age. 12 (50%) had multiple episodes of hypoglycemia. 3 babies were symptomatic and required intravenous fluid therapy. Rest were managed with supplementary oral feeds. Of 14 babies with polycythemia, only 3 were symptomatic. Polycythemia was detected at 2 h in 50%, at 6 h in 29%, at 12 h in 14% and only 7% at 24 h of life. No cases of polycythemia were detected at 48 and 72 h of life. Management Early delivery is indicated if there is arrest of fetal growth and pulmonary maturity is satisfactory. Fetal hypoxia may necessitate emergency cesarean section and one should be prepared to receive an asphyxiated infant. If liquor is meconium stained and the neonate is depressed, endotracheal suctioning is essential10. Infant should be screened for any congenital malformations. Based on initial assessment, decision is taken to either keep the infant in nursery or with mother. Birth weight 3rd – 10th percentile

Downloaded from www.newbornwhocc.org 5 AIIMS- NICU protocols 2007 In the absence of complications including perinatal asphyxia and respiratory distress, these neonates may be managed with the mother (Table 2). Skin-to-skin care helps in maintaining temperature and facilitates breast-feeding. Early initiation of breastfeeding and/ or assisted feeding helps in averting hypoglycemia. Term SGA infants usually do not pose any serious difficulties because they have no problems in direct breast-feeding. To avoid hypoglycemia, they should be put to breast within one hour of birth. However these infants are at risk of morbidities and should be monitored regularly for hypoglycemia and polycythemia in the first 48-72 hours. Neonates with asymptomatic hypoglycemia should be supplemented with sugar fortified formula feeds. This may be given with the help of a cup and spoon/ paladai. Neonates with normoglycemia on regular feeds should be gradually weaned to exclusive breast-feeding within the next 3-4 days. Failure to maintain normoglycemia despite regular oral feeds should be treated with IV fluids. Neonates with symptomatic hypoglycemia should be shifted to a special care nursery and managed appropriately with a glucose bolus followed by a continuous glucose infusion at 6-8 mg/kg/min. Neonates with asymptomatic polycythemia and a hematocrit <75 maybe managed conservatively by increasing fluid intake. The infant should receive regular (2-3 hourly) breast feeds with extra supplementation. Infants with symptomatic polycythemia or hematocrit >75 should be managed by partial exchange transfusion in the neonatal intensive care unit11. Birth weight <3rd percentile, gestation <35 weeks Neonates with severe growth restriction (<3rd percentile) or with presence of complications should be managed in the intensive care unit (Table 2). This group would include infants with perinatal asphyxia, symptomatic hypoglycemia, symptomatic polycythemia, prematurity (<35 weeks), respiratory distress and hypothermia. They should be monitored for hypoglycemia, polycythemia and feed intolerance in the initial few days. Downloaded from www.newbornwhocc.org 6

AIIMS- NICU protocols 2007 Infants with gestation <30 weeks (birth weight <1200 grams) should be started on IV fluids initially and gradually weaned to oral feeds over the next few days. In the absence of other complications, oro-gastric feeds should be started for neonates >30 weeks (>1200 grams) and gradually shifted to katori-spoon/ paladai feeding. An infant on full oral feeds with spoon-feeding may be tried on direct breast-feeding. These high-risk infants need to be observed for a minimum of 72 hours for hypoglycemia. Infants on full katori-spoon feeding and/ or breast-feeding may be shifted to the mother after 72 hours if she is confident of on going-care. Paladai/ spoon feeding Feeding with a spoon (or a similar device such as ‘paladai’) and katori (or any other receptacle such as cup) has been found to be safe in SGA infants8. This mode of feeding is a bridge between gavage feeding and direct breast-feeding. It is based on the premise that neonates with a gestation of 30-32 weeks or more are in a position to swallow the feeds satisfactorily even though they may not be good at sucking or coordinated sucking and swallowing. A medium sized katori and a small (1-2 ml size) spoon should be used. The spoon should be filled just short of the brim with expressed milk, should be placed at the corner of mouth and milk should be allowed to flow into the infant’s mouth slowly, avoiding any spillage. The infant would actively swallow the milk. This process should be repeated till the required amount has been fed. If the infant does not actively accept and swallow the feed, an attempt should be made to wake the infant with gentle stimulation. If he is still sluggish, do not insist on this method. It is better to switch back to gavage feeds till the infant is ready. SGA/IUGR babies with absent or reversed end-diastolic flow (AREDF) in umbilical artery In the IUGR fetus, hypoxaemia produces circulatory redistribution towards the brain and away from the viscera and placenta, culminating in umbilical artery or aortic AREDF in the most Downloaded from www.newbornwhocc.org 7 AIIMS- NICU protocols 2007

severely affected fetuses. The combination of antenatal and persisting postnatal disturbances of gut perfusion, interacting with the metabolic demands of feeding, may adversely affect intestinal tissue oxygenation, combining with stasis and immunological factors to contribute to the development of NEC. A review by Dorling et al including 14 studies and 1178 neonates found higher risk of NEC in IUGR babies with AREDF (odds ratio: 2.13; 95% CI: 1.49 to 3.03).12 Although evidence for feeding strategy to be adopted in these babies is limited, it may be prudent to start and persist with minimal enteral nutrition for first 48-72 h of life. Long-term outcome and follow-up IUGR babies are at risk for poor growth and neuro-developmental outcome.3 We routinely follow IUGR babies with birthweight below <3rd percentile and those with birthweight 3-10th percentile if they develop significant morbidities (e.g. hypoglycemia, polycythemia, birth asphyxia) during hospital stay. Downloaded from www.newbornwhocc.org 8 AIIMS- NICU protocols 2007 References 1. United Nations Childrens Fund and World Health Organization, Low Birthweight: Country,regional and global estimates. UNICEF, New York, 2004. 2. Arora NK, Paul VK, Singh M. Morbidity and mortality in term infants with intrauterine growth retardation. J Trop Pediatr 1987;33: 186-9. 3. Teberg AJ, Walther FJ, Pena IC. Mortality, morbidity, and outcome of the small-for-gestationalage preterm infant. Semin Perinatol 1988;12: 84-94. 4. Mavalankar DV, Gray RH, Trivedi CR, Parikh VC. Risk factors for small for gestational age births in Ahmedabad, India. J Trop Pediatr 1994;40:285-90. 5. Arora NK, Singh M, Paul VK, Bhargava VL. Etiology of fetal growth retardation in hospital born infants. Indian J Med Res 1987;85:395-400. 6. Bhatia BD, Agarwal KN, Jain NP, Bhargava V. Growth pattern of intrauterine growth retarded (IUGR) infants in first nine months of life. Acta Pediatr Scand 1984;73:189-96. 7. Singh M. Disorders of weight and gestation. In Care of the Newborn (Ed) Singh M. 5th Ed, 1999, Sagar Publications, New Delhi pp 224-45.

8. Singh M, Giri SK, Ramachandran K. Intrauterine growth curves of live-born infants. Indian Pediatr 1974;11: 475-9. 9. Paul VK. Management of LBW babies. In NNF Teaching Aids on Newborn Care. Ed Deorari AK. 2nd Ed, 1998, Noble Vision, New Delhi pp 25-36 10. Niermayer S, Kattwinkel J, Van Reempts P, Nadkarni V, Phillips B, Zideman D et al. International guidelines for neonatal resuscitation. An excerpt from the guidelines 2000 for cardiopulmonary resuscitation and emergency cardiovascular care. International consensus on Downloaded from www.newbornwhocc.org 9 AIIMS- NICU protocols 2007 Science. Contributors and reviewers for the neonatal resuscitation guiidelines. Pediatrics 2000;106:E29. 11. Deorari AK, Paul VK, Shrestha L, Singh M. Symptomatic neonatal polycythemia: comparison of partial exchange transfusion with saline versus plasma. Indian Pediatr 1995;32: 1167-71 12. Dorling J, Kempley S, Leaf A. Feeding growth restricted preterm infants with abnormal antenatal Doppler results. Arch Dis Child Fetal Neonatal Ed. 2005;90:F35963. Downloaded from www.newbornwhocc.org 10 AIIMS- NICU protocols 2007

Table 1: Common morbidities in SGA neonates Period: Jan 1999 to Dec 00 (n=156) Period: Aug 04 to Jul 05 (n=144) Weight <3rd percentile (n=47) Weight 3rd-10th percentile (n=109) Weight <10th percentile (n=144) Birth asphyxia Total

Moderate Severe 4 (8.5%) 22 10 (9.2%) 82 25 (17%) -Hypoglycemia Total Symptomatic Asymptomatic 12 (25.5%) 66 14 (12.8%) 3 11 24 (17%) 3 21 Polycythemia Total Symptomatic Asymptomatic 14 (29.8%) 3 11 17 (15.6%) 89 14 (10%) 3 11 Hypothermia 0 4 (3.7%) 19* (13.2%) *Includes 1 baby with hypothermia and 18 babies with cold stress
Downloaded from www.newbornwhocc.org 11 AIIMS- NICU protocols 2007

Table 2: Management of SGA infants Criteria for admission to Nursery - All SGA infants < 2 SD (3rd percentile) - Infants with gestational age < 35 wks

- Infants with birth asphyxia, respiratory distress etc. Care of SGA infants with mothers (birth weight between 3rd and 10th percentile, gestation >35 wks) • Early initiation of breast feeding (within 1 hour) • Skin-to-skin care to maintain temperature, monitoring of cold stress by mother and health professionals. • Monitor blood sugar, hematocrit • Prevent infections Care of SGA infants in Nursery (birth weight <3rd percentile or gestation <35 wks) • Nurse in thermo neutral environment • It stable, early initiation of feeds ( EBM). - Feed by orogastric tube or katori-spoon /paladai if gestation >32 wks - Initial intravenous fluids followed by orogastric or katorispoon /paladai if gestation <32 wks • Monitor blood sugar, hematocrit Care of SGA infants with absent or reversed en-diastolic blood flow • At higher risk of development of NEC • If preterm (gestation <32 weeks): Nil per oral or on minimal enteral nutrition for first 48-72 h of life followed by gradual advancement of feed volume
Downloaded from www.newbornwhocc.org 12 AIIMS- NICU protocols 2007

Figure 1: Algorithm for management of SGA infants
SGA* Term (borderline) <35 wk <3rd percentile 3rd –10th percentile Admit nursery Monitor with mother Admit nursery Breastfeeding or katori-spoon Breastfeeding <30 wk – initial on IV 30 – 34 wk orogastric or katori-spoon *Blood sugar, hematocrit, temperature monitoring
Downloaded from www.newbornwhocc.org 13

PREMATURITY AND IUGR
The causes of neonatal hypoglycemia can be categorized according to associated disturbances in one or more of the processes required for normal hepatic glucose production that may lead to transient or prolonged episodes of hypoglycemia (Table 1 ). Hepatic glycogen stores are limited in both preterm infants, who have not experienced the period of rapid glycogen accumulation during late gestation, and small-for-gestational age (SGA) infants, who have not had adequate substrate supply available for glycogen synthesis, which puts these newborns at risk for hypoglycemia. IUGR due to placental insufficiency with preservation of normal head size puts an added demand on the infant's already low glycogen stores because of the increased brain-to-bodyweight ratio. Postterm infants and infants of multiple gestations also may be at risk because of the presence of relative placental insufficiency. In addition to decreased glycogen availability, studies in preterm and IUGR infants have found altered patterns of insulin secretion, substrate metabolism, and hormonal responses to changes in blood glucose concentration compared with appropriate-for-gestational age (AGA) term infants.

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High-Risk Pregnancy
Intrauterine Growth Restriction (IUGR)
What is intrauterine growth restriction (IUGR)?

Intrauterine growth restriction (IUGR) is a term used to describe a condition in which the fetus is smaller than expected for the number of weeks of pregnancy. Another term for IUGR is fetal growth restriction. Newborn babies with IUGR are often described as small for gestational age (SGA). A fetus with IUGR often has an estimated fetal weight less than the 10th percentile. This means that the fetus weighs less than 90 percent of all other fetuses of the same gestational age. A fetus with IUGR also may be born at term (after 37 weeks of pregnancy) or prematurely (before 37 weeks). Newborn babies with IUGR often appear thin, pale, and have loose, dry skin. The umbilical cord is often thin and dull-looking rather than shiny and fat. Babies with IUGR sometimes have a wide-eyed look. Some babies do not have this malnourished appearance but are small all-over.
What causes intrauterine growth restriction (IUGR)?

Intrauterine growth restriction results when a problem or abnormality prevents cells and tissues from growing or causes cells to decrease in size. This may occur when the fetus does not receive the necessary nutrients and oxygen needed for growth and development of organs and tissues, or because of infection. Although some babies are small because of genetics (their parents are small), most IUGR is due to other causes. Some factors that may contribute to IUGR include the following:



Maternal factors: ○ ○ ○ ○ ○ ○ ○ ○ high blood pressure chronic kidney disease advanced diabetes heart or respiratory disease malnutrition, anemia infection substance abuse (alcohol, drugs) cigarette smoking



Factors involving the uterus and placenta: ○ ○ decreased blood flow in the uterus and placenta placental abruption (placenta detaches from the uterus) placenta previa (placenta attaches low in the uterus) infection in the tissues around the fetus


○ •

Factors related to the developing baby (fetus):


○ ○

multiple gestation (twins, triplets, etc.) infection birth defects



chromosomal abnormality

Why is intrauterine growth restriction (IUGR) a concern?

IUGR can begin at any time in pregnancy. Early-onset IUGR is often due to chromosomal abnormalities, maternal disease, or severe problems with the placenta. Late-onset growth restriction (after 32 weeks) is usually related to other problems. With IUGR, the growth of the baby's overall body and organs are limited, and tissue and organ cells may not grow as large or as numerous. When there is not enough blood flow through the placenta, the fetus may only receive low amounts of oxygen. This can cause the fetal heart rate to decrease placing the baby at great risk. Babies with IUGR may have problems at birth including: • decreased oxygen levels low Apgar scores (an assessment that helps identify babies with difficulty adapting after delivery) meconium aspiration (inhalation of the first stools passed in utero), which can lead to difficulty breathing hypoglycemia (low blood sugar) difficulty maintaining normal body temperature polycythemia (too many red blood cells)

• •
• •



Severe IUGR may result in stillbirth. It may also lead to long-term growth problems in babies and children.
How is intrauterine growth restriction (IUGR) diagnosed?

During pregnancy, fetal size can be estimated in different ways. The height of the fundus (the top of a mother's uterus) can be measured from the pubic bone. This measurement in centimeters usually corresponds with the number of weeks of pregnancy after the 20th week. If the measurement is low for the number of weeks, the baby may be smaller than expected. Other diagnostic procedures may include the following:



ultrasound Ultrasound (a test using sound waves to create a picture of internal structures) is a more accurate method of estimating fetal size. Measurements can be taken of the fetus' head and abdomen and compared with a growth chart to estimate fetal weight. The fetal abdominal circumference is a helpful indicator of fetal nutrition. Doppler flow Another way to interpret and diagnose IUGR during pregnancy is Doppler flow, which use sound waves to measure blood flow. The sound of moving blood produces wave-forms that reflect the speed and amount of the blood as it moves through a blood vessel. Blood vessels in the fetal brain and the umbilical cord blood flow can be checked with Doppler flow studies. mother's weight gain A mother's weight gain can also indicate a baby's size. Small maternal weight gains in pregnancy may correspond with a small baby.





How is intrauterine growth restriction (IUGR) managed?

Management of IUGR depends on the severity of growth restriction, and how early the problem began in the pregnancy. Generally, the earlier and more severe the growth restriction, the

greater the risks to the fetus. Careful monitoring of a fetus with IUGR and ongoing testing may be needed. Some of the ways to watch for potential problems include the following:

• • • •

fetal movement counting - keeping track of fetal kicks and movements. A change in the number or frequency may mean the fetus is under stress. nonstress testing - a test that watches the fetal heart rate for increases with fetal movements, a sign of fetal well-being. biophysical profile - a test that combines the nonstress test with an ultrasound to evaluate fetal well-being. ultrasound - a diagnostic imaging technique which uses high-frequency sound waves and a computer to create images of blood vessels, tissues, and organs. Ultrasounds are used to view internal organs as they function, and to assess blood flow through various vessels. Ultrasounds are used to follow fetal growth. Doppler flow studies - a type of ultrasound which use sound waves to measure blood flow.



Treatment for IUGR:

Although it is not possible to reverse IUGR, some treatments may help slow or minimize the effects. Specific treatments for IUGR will be determined by your physician based on: • • • • • your pregnancy, overall health, and medical history the extent of the disease your tolerance for specific medications, procedures, or therapies expectations for the course of the disease your opinion or preference nutrition Some studies have shown that increasing maternal nutrition may increase gestational weight gain and fetal growth. bedrest Bedrest in the hospital or at home may help improve circulation to the fetus. delivery If IUGR endangers the health of the fetus, then an early delivery may be necessary.

Treatments may include:



• •

Prevention of intrauterine growth restriction:

Intrauterine growth restriction may occur, even when the mother is in good health. However, some factors may increase the risks of IUGR, such as cigarette smoking and poor maternal nutrition. Avoiding harmful lifestyles, eating a healthy diet, and getting prenatal care may help decrease the risks for IUGR. Early detection may also help with IUGR treatment and outcome. Click here to view the Online Resources page of this Web Site.
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Abnormal size at birth

D: SGA: birth weight < 20th percentile for gestational age or < 2.5 kg. LGA: birth weight > 90th percentile for gestational age or > 4 kg. A: SGA: may be familial, constitutional, or due to IUGR. IUGR is defined as either symmetrical or asymmetrical: Asymmetrical IUGR: relative sparing of head circumference in relation to weight and length: . Due to impaired uteroplacental function 28 to maternal pre-eclampsia, DM or nutritional deficiency during the 3rd trimester. . Occurs when foetal growth rate in 3rd trimester exceeds maximal supply from the placenta. . There is preferential sparing of the cerebral perfusion at times of foetal distress. Symmetrical IUGR: head circumference, weight, and length are all proportionally affected to equivalent degrees: . Indicative of a prolonged period of poor intrauterine growth. . Caused by congenital intrauterine infections (TORCH) in the 1st trimester, genetic factors such as single gene deletions and chromosomal disorders, maternal smoking, drug and alcohol abuse, chronic medical conditions (e.g. CRF), malnutrition, or multiple pregnancies. LGA: macrosomia is a feature of infants of mothers with either gestational or poorly controlled/undiagnosed DM. A/R: IUGR: previous SGA infant, low pre-pregnancy weight and poor pregnancy weight gain. E: SGA: affects by definition 20% of the population and varies with ethnic background. IUGR: 2/200 neonates; asymmetrical > symmetrical IUGR. LGA: affects by definition 20% of live births; is more common in developed countries where there is a higher prevalence of DM. H& E: Antenatal: maternal examination and accurate dating aid diagnosis. Oligohydramnios and poor foetal movements are indications of placental insufficiency. Perinatal monitoring: foetal tachycardia, loss of variability of the baseline in the foetal heart trace, and late decelerations may indicate foetal distress on CTG. Postnatal measurements: birth weight, length, and head circumference on centile chart. P: See A. I: Radiology: USS is the 18 method of diagnosing IUGR or macrosomia antenatally. Cordocentesis: percutaneous umbilical blood sampling may be used for detection of hypoxia, lactic acidosis, hypoglycaemia, chromosomal analysis, and DNA diagnosis of congenital intrauterine infections. M: Antenatal: maternal bedrest and limitation of activity for severe IUGR. Perinatal: maternal administration of O2, continuous assessment of foetal well-being. Delivery (IUGR): if foetus becomes hypoxic in utero, an emergency

Caesarean section is required. Macrosomia: induce at 38/40 to prevent complications in a unit with good neonatal facilities. 3

CONDITIONS

Abnormal size at birth continued

C: IUGR foetus: intrauterine hypoxia, birth asphyxia, and death. IUGR infant: hypothermia (relatively large surface area), hypoglycaemia (poor fat and glycogen stores), hypocalcaemia, polycythaemia, and meconium aspiration. LGA: birth asphyxia due to prolonged/difficult delivery, birth trauma, especially shoulder dystocia, hypoglycaemia in the neonatal period due to hyperinsulinism, and polycythaemia. P: Depends on the cause of abnormal size at birth. Infants with asymmetrical IUGR will rapidly put on weight in the postnatal period; symmetrical IUGR infants are more likely to remain small permanently. Studies have shown that IUGR infants are at "risk of developing "BP, Type II DM, and coronary heart disease. 4

CONDITIONS
Acne vulgaris

D: Inflammation of the pilosebaceous duct. Classified as mild, moderate, and severe. A: Adolescent acne: . "Sebum production: androgenic stimulation of hyper-responsive pilosebaceous units. . Impaired normal flow of sebum: obstruction of the pilosebaceous duct by hyperkeratosis. . Propioni acne bacteria: may play a role by producing cytokines and lipolytic enzymes. Infantile acne: <3 months of life; transient and usually due to maternal androgens. A/R: Puberty, may " premenstrually, POS, excess cortisol (Cushing syndrome). E: Developed world: affects 79–95% of the adolescent population, peaking at 14–18 years; tends to recede by early twenties. Developing world: acne incidence is considerably lower; likely combination of environmental and genetic factors. H: Usually self-diagnosed, acute onset, greasy skin, may be painful. E: Open comedones: whiteheads; flesh-coloured papules. Closed comedones: blackheads; black colour is due to oxidation of the melanin pigment. Other features: pustules, nodules, cysts, scarring, and seborrhoea. Distribution: primarily affects the face, neck, chest, and back (where sebaceous glands are most numerous). P: Gross distension of the pilosebaceous follicle with neutrophil infiltration. Closed comedones may contain serous fluid. Severe acne can create fistulae between inflamed glands. I: Normally none required. Investigate for endocrine disorder if acne develops during 2–10 years of age. Bloods: FSH, LH (if female, suspect POS). Urine: 24-h-urinary cortisol (if Cushing syndrome is suspected). M: Many cases may not need treatment. Indication for treatment based on classification and degree of psychosocial impact. In severe acne, therapy should be commenced early to prevent scarring. Topical preparations: (1) Benzoyl peroxide; keratolytic agent, encourages skin peeling, and # number of P. acnes (S/E: irritation and bleaching of clothes). (2) Vitamin A derivatives; tretinoin, may take 3–4 months to work. (3) Azelaic acid. Antibiotics: (1) Topical: clindamycin, erythromycin. (2) Systemic: tetracycline only in > 16 years. (S/E: discolours teeth and may soften bones in children.) A gradual " in P. acne resistance to many antibiotics has been documented; growing need to use either appropriate antibiotics or change the therapeutic strategy in favour of other regimens. Isotretinoin (Roaccutane P.O.): vitamin A derivative, 4–6-month course only by specialist prescription for severe acne (S/E: teratogenic; females require OCP, hyperlipidaemia). Antiandrogens: in females only; OCP or cyproterone acetate. UVB: adjunctive therapy, but rarely used. Advice: improvement may not be seen for at least a couple of months, use nongreasy cosmetics, wash face daily, moderate exposure to sunshine is beneficial. 5

CONDITIONS
Acne vulgaris continued
C: Physical: facial scarring (atrophic/keloid), hyperpigmentation of scars, 28 infection and fistulae. Psychosocial: lack of self-confidence. P: Generally improves spontaneously over months/years. Persists into adulthood in 22% of women and 3% of men. 6

CONDITIONS

Acquired female genital disorders

D: Abnormalities of the female genital tract not present at birth. A: Labial adhesions: adherence of the labia minora in the midline; may give the appearance of absence of the vagina. A thin pale semi-translucent membrane covers the vaginal os. Trauma causes denudation of the epithelial layer of the labia minora mucosa and leads to fibrous tissue formation; therefore sealing of the labia minora. Trauma can involve inflammatory conditions (vulvitis, vulvovaginitis), sexual abuse, or straddle injuries. Vulvovaginitis: pruritus, vulval pain, vulval erythema, vaginal discharge or bleeding. Usually associated with poor perineal hygeine, constipation, and atopic dermatitis caused by local irritants (bubble bath, soaps, shampoo) or by occlusive clothing causing irritation. May be caused by trauma 28 to abuse; therefore this should be considered if other concerns are present. A/R: Vulvovaginitis is often misdiagnosed as a UTI due to its similar presentation. E: Labial adhesions: peak age: 3 months to 6 years, incidence: 1–2%. Vulvovaginitis: very common in <5-year-olds. H: Labial adhesions: usually asymptomatic and noted on routine examination. Some patients may leak urine when they stand after voiding. Vulvovaginitis: history should include toilet-training, type of nappy used, bad odour or dark discharge, scratching, history of eczema, allergic rhinitis, or diarrhoea, tendency of child to insert objects, and any possible indication of abuse. E: General: should be by a skilled clinician, in a well-lit room with a relaxed and distracted child (mother reading book). Labial adhesions: the edges of the labia minora are sealed along the midline, beginning at the posterior fourchette and extending anteriorly towards the clitoris. Vulvovaginitis: commonly, only vulvitis will be detected, although vaginal discharge and bleeding may also be present. P: See A. I: Exclude other vaginal disorders such as imperforate hymen or septate vagina prior to treatment. Microbiology: vaginal swab if discharge present, MSU. Radiology: indirect cystourethrogram may show urinary retention behind the fused labia, bladder distention þ=_ hydronephrosis in labial adhesions. M: Labial adhesions: oestrogen cream dissolves the adhesions in 90% of cases. Once adhesions have been lysed vasoline is used as prophylaxis for 1–2 months. Vulvovaginitis: . Treat any underlying infection with appropriate antibiotics. . Education of adequate perineal hygiene and removal of potential irritants. C: Labial adhesions: without adequate treatment 20–40% will develop UTI. P: Labial adhesions: recurrence is common, therefore good follow-up is required. Vulvovaginitis: outcome good with improved perineal hygiene. 7

CONDITIONS

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Intrauterine Growth Retardation
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).

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▪ Baby Shower Description Games ▪ There are standards or averages in weight for unborn babies according their age in weeks. When the baby's weight is at or below the 10th percentile for his Pregnancy or her age, it is called intrauterine growth retardation or fetal growth restriction. Website These babies are smaller than they should be for their age. How much a baby ▪ Pregnancy weighs at birth depends not only on how many weeks old it is, but the rate at Signs which it has grown. This growth process is complex and delicate. There are ▪ three phases associated with the development of the baby. During the first Pregnancy phase, cells multiply in the baby's organs. This occurs from the beginning of

development through the early part of the fourth month. During the second Problem phase, cells continue to multiply and the organs grow. In the third phase (after ▪ 32 weeks of development), growth occurs quickly and the baby may gain as Flatulence much as 7 ounces per week. If the delicate process of development and Causes weight gain is disturbed or interrupted, the baby can suffer from restricted growth. ?My Word List IUGR is usually classified as symmetrical or asymmetrical. In symmetrical IUGR, the baby's head and body are proportionately small. In asymmetrical Add current page to the IUGR, the baby's brain is abnormally large when compared to the liver. In a list normal infant, the brain weighs about three times more than the liver. In Advertisement (Bad asymmetrical IUGR, the brain can weigh five or six times more than the liver. banner? Please let us Causes and symptoms know) Doctors think that the two types of IUGR may be linked to the time during ?Charity development that the problem occurs. Symmetrical IUGR may occur when the Feed a unborn baby experiences a problem during early development. Asymmetrical hungry child IUGR may occur when the unborn baby experiences a problem during later - donate to development. While not true for all asymmetrical cases, doctors think that school feeding program sometimes the placenta may allow the brain to get more oxygen and nutrition while the liver gets less. There are many IUGR risk factors involving the mother and the baby. A mother is at risk for having a growth restricted infant if she: • • Has had a previous baby who suffered from IUGR Is small in size Has poor weight gain and nutrition during pregnancy Is socially deprived Uses substances (like tobacco, narcotics, alcohol) that can cause abnormal development or birth defects Has a vascular disease (like preeclampsia) Has chronic kidney disease Has a low total blood volume during early pregnancy Is pregnant with more than one baby Has an antibody problem that can make successful pregnancy difficult (antiphospholipid antibody syndrome). Exposure to an infection, including German measles (rubella), cytomegalovirus, tuberculosis, syphilis, or toxoplasmosis A birth defect (like a severe cardiovascular defect) A chromosome defect, especially trisomy 18 (Edwards' syndrome) A primary disorder of bone or cartilage A chronic lack of oxygen during development (hypoxia) Placenta or umbilical cord defects Developed outside of the uterus. Advertisement (Bad banner? Please let us know)








• •



Additionally, an unborn baby may suffer from IUGR if it has:





• • • •

Key terms
Preeclampsia — Hypertension (high blood pressure) during pregnancy.

Diagnosis
IUGR can be difficult to diagnose and in many cases doctors are not able to make an exact diagnosis until the baby is born. A mother who has had a growth restricted baby is at risk of having another during a later pregnancy. Such mothers are closely monitored during pregnancy. The length in weeks of the pregnancy must be carefully determined so that the doctor will know if development and weight gain are appropriate. Checking the mother's weight and abdomen measurements can help diagnose cases when there are no other risk factors present. Measuring the girth of the abdomen is often used as a tool for diagnosing IUGR. During pregnancy, the healthcare provider will use a tape measure to record the height of the upper portion of the uterus (the uterine fundal height). As the pregnancy continues and the baby grows, the uterus stretches upward in the direction of the mother's head. Between 18 and 30 weeks of gestation, the uterine fundal height (in cm.) equals the weeks of gestation. If the uterine fundal height is more than 2-3 cm below normal, then IUGR is suspected. Ultrasound is used to evaluate the growth of the baby. Usually, IUGR is diagnosed after week 32 of pregnancy. This is during the phase of rapid growth when the baby should be gaining more weight. IUGR caused by genetic factors or infection may sometimes be detected earlier.

Treatment
There is no treatment that improves fetal growth, but IUGR babies who are at or near term have the best outcome if delivered promptly. 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.

Prognosis
Babies who suffer from IUGR are at an increased risk for death, low blood sugar (hypoglycemia), low body temperature (hypothermia), 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. However, as of 1998, doctors cannot reliably predict an infant's future progress. Each case is unique. Some infants who have IUGR will develop normally, while others will have complications of the nervous system or intellectual problems like learning disorders. 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.

Resources
Books Cunningham, F. Gary, et al. Williams Obstetrics. 20th ed. Stamford: Appleton & Lange, 1997.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.

intrauterine growth retardation
n. Abbr. IUGR

Birth weight that is below the tenth percentile for gestational age. Also called intrauterine growth restriction.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

intrauterine growth retardation,
an abnormal process in which the development and maturation of the fetus are impeded or delayed more than two deviations below the mean for gestational age, sex, and ethnicity. It may be caused by genetic factors, maternal disease, or fetal malnutrition that results from placental insufficiency. See also growth retardation, small for gestational age infant.
Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

intrauterine
within the uterus. intrauterine contraceptive device a mechanical device inserted into the uterine cavity for the purpose of contraception. These devices, used in human gynecology, have been used in draft cattle in Asia for many years. Used occasionally also in dogs. Called also IUD. intrauterine growth retardation failure to grow properly in utero in stature, as measured by crown to rump measurement. Pituitary dwarfism in cattle and runting in piglets and puppies are typical examples. intrauterine medication medication applied to the uterus via a cervical catheter, or manually in the recently birthed mare, sow or cow. intrauterine therapy is a common practice in food animals. Infusion of fluid material or manual placement of solid materials are the usual methods employed. The method has the advantage of achieving maximum concentration of the medicament at the endometrium but only low concentrations are achieved in the deeper layers. See also infusion.
Saunders Comprehensive Veterinary Dictionary, 3 ed. © 2007 Elsevier, Inc. All rights reserved

intrauterine growth retardation
Fetal growth restriction Neonatology A generic term for any delay in achieving intrauterine developmental milestones, most commonly related to maternal drug, tobacco and alcohol abuse; IUGR affects high-risk infants with perinatal asphyxia, hypoglycemia, hypothermia, pulmonary hemorrhage, meconium aspiration, necrotizing enterocolitis, polycythemia and complications of infections, malformations and syndromes; IUGR fetuses have weight < 10th percentile for gestational age, abdominal circumference < 2.5th percentile Types Symmetric–body is proportionately small; asymmetric–head is disproportionately bigger than body, which implies undernourishment–growth of vital organs–heart, brain is at expense of liver, muscle and fat, often due to placental insufficiency; IUGR is the 2nd most common–after prematurity–cause of perinatal M&M; it affects ±5% of the general obstetric population. See Low birthweight, Small for gestational age.

Intrauterine growth restriction Placental insufficiency • Unexplained elevated maternal alpha- fetoprotein level • Idiopathic • Preeclampsia • Chronic maternal disease • Cardiovascular disease • Diabetes • Hypertension Abnormal placentation • Abruptio placentae • Placenta previa • Infarction • Circumvallate placenta • Placenta accretia • Hemangioma Genetic disorders • Family history • Trisomy 13, 18 and 21 • Triploidy • Turner's syndrome (some cases) • Malformations Immunologic • Antiphospholipid syndrome Infections • Cytomegalovirus • Rubella • Herpes • Toxoplasmosis Metabolic • Phenylketonuria Other • Poor maternal nutrition • Substance abuse (smoking, alcohol, drugs) • Multiple gestation • Low socioeconomic status
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

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References in periodicals archive

Antepartum Testing expanded rubella syndrome FGR growth retardation High-risk pregnancy Intrauterine growth restriction IUGR low birth weight placental insufficiency preeclampsia

Fetal transfusion syndrome, fetofetal transfusion syndrome, stuck twin syndrome Obstetrics Intrauterine growth retardation in 1 twin due to an artery-to-artery vascular shunting, which may occur in a diamnionic-dichorionic placenta Hemodynamics and cardiology; neonatology questions and controversies by SciTech Book News We found evidence of associations between exposure to specific HAAs and term low birth weight as well as intrauterine growth retardation and for exposure to the five regulated HAAs (HAAS) and term low birth weight. Late pregnancy exposures to disinfection byproducts and ... by Reif, John S. / Environmental Health Perspectives Every 17 parts per billion increase in daily ozone levels during a woman's third trimester increases the risk of intrauterine growth retardation by 20 percent. OZONE LEVEL POSES RISK TO WOMEN BABIES BORN UNDERWEIGHT by Daily News (Los Angeles, CA) More results

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Causes and Symptoms The two types of IUGR described previously contribute to IUGR according to the development at that stage. Symmetrical IUGR may occur when the unborn baby experiences a problem during early development. Asymmetrical IUGR may occur when the unborn baby experiences a problem during later development. In general, most physicians believe that IUGR is the consequence of a disease process within one or more of the three partitions that maintain and regulate fetal growth, i.e., the maternal compartment, the placenta, or the fetus. In consideration of risk factors uteroplacental insufficiency contributes to 80 percent of IUGR due to the following maternal causes:

• • • • • • • • •

deficient supply of nutrients smoking malnutrition anemia drug abuse vascular diseases, i.e., high blood pressure chronic kidney disease severe diabetes multiple gestation

Intrauterine growth retardation (IUGR) Conditions associated with IUGR Maternal history Alcohol use Cocaine use Smoking Malnutrition Use of prescription drugs warfarin (Coumadin, Panwarfarin) and phenytoin (Dilantin) Prior history of IUGR pregnancy Residing at altitude over 5,000 ft (1,500 m) Medical conditions (of mother) Chronic hypertension Preeclampia early in gestation Diabetes mellitus Systemic lupus erythematosus Chronic kidney disease Inflammatory bowel disease Severe lung disease Infectious diseases Syphilis Cytomegalovirus Toxoplasmosis Rubella Hepatitis B Herpes simplex virus 1 or 2 HIV-1 Congenital disorders (of fetus) Trisomy 21 (Down syndrome) Trisomy 18 (Edwards syndrome) Trisomy 13 (Patau syndrome) Turner's syndrome
• •

antigen/antibody reactions, i.e., lupus, antiphospholipid antibody syndrome (APA) primary placental causes, i.e., extensive placental infarctions, chronic placental separation, placenta previa

Primary fetal causes contribute to 20 percent of IUGR and include the following:

• • • • •

exposure to an infection, i.e., rubella (German measles), cytomegalovirus, syphilis, or toxoplasmosis birth defects, i.e., congenital heart disease, genitourinary anomalies, central nervous system defects chromosomal abnormalities, i.e., trisomy 13, 18, or 21 primary bone or cartilage disorder decreased intrinsic growth, symmetrical IUGR

While most fetuses with IUGR usually have no complications, there is an increased risk for intrapartum asphyxia, neonatal hypoglycemia and hypocalcemia, meconium aspiration, and neurodevelopmental delays. The following summarizes these complications:

Intrapartum Asphyxia
Because the fetus is compromised with IUGR, its ability to tolerate the stress of labor is decreased. Therefore, when uterine contractions occur and the flow of blood to the fetus is diminished with each contraction, the fetus with IUGR may not be able to adapt. This leads to an imbalance between the ability of the placenta to supply the fetus with oxygen and nutrients and the need for these substances. When an imbalance occurs, this may lead to an accumulation of

byproducts resulting in acidosis which can be harmful. If intrapartum asphyxia is allowed to progress, irreversible brain damage can occur. Medical Literature

Neonatal Hypoglycemia and Hypocalcemia
As the result of IUGR, a newborn may be deficient in glucose (sugar) and calcium. The lack of these important substances can result in significant compromise to the newborn and result in neurological damage. Medical Literature Medical Literature

Meconium Aspiration
This occurs when the fetus defecates in the uterus resulting in the appearance of a brown, murky substance. Since the contents from the fetal bowel contains many substances that can be harmful to the fetus if swallowed, meconium aspiration is of major concern. In severe forms, the newborn may develop lung disease resulting in respiratory and cardiovascular complications that could lead to neonatal death. Medical Literature

Neurodevelopmental Delay
A number of studies have shown that fetuses with significant IUGR are at higher risk for developmental delays, cardiovascular disease, and other problems later in life. For these reasons, and those stated above, it is important to identify the fetus with IUGR and manage the pregnancy accordingly Medical Literature

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