Extremely Low Birth Weight Gopal

8/13/2019 Extremely Low Birth Weight Gopal

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EXTREMELY LOW BIRTH WEIGHT (ELBW)

Overview

An extremely low birth weight (ELBW) infant is defined as one with a birth weight of less than1000g (2lb, 3oz). Most extremely low birth weight infants are also the youngest of premature

newborns, usually born at 27 weeks' gestational age or younger. Infants born at less than 1500gare defined as having very low birth weight (VLBW).

Low birth weight (< 2500g) was noted in 8.3% of all births in the United States in 2006, andvery low birth weight was noted in 1.48% of all births; approximately 63,137 US births werereported in 2006.[1]

Infants whose weight is appropriate for their gestational ages are termed appropriate forgestational age (AGA). Infants who are heavier than expected are large for gestational age(LGA); conversely, those smaller than expected are considered small for gestational age (SGA)and are also usually found to be intrauterine growth restricted (IUGR) prior to birth.

Extremely low birth weight survival has improved with the widespread use of surfactant agents,

maternal steroids, and advancements in neonatal technologies. The minimum age of viability isnow as young as 23 weeks' gestation, with scattered reports of survivors born at 21-22 weeks'estimated gestation.

Morbidity and Mortality

Survivability correlates with gestational age for infants who are appropriate for gestational age(AGA). In 2002, the first-year survival rate was 13.8% for infants with a birth weight of less than500 g, 51% for infants with a birth weight of 500-749g, and 84.5% for infants with a birth weightof 750-1000g. Infants with extremely low birth weight (ELBW) are more susceptible to all of thepossible complications of premature birth, both in the immediate neonatal period and afterdischarge from the nursery.

Although the mortality rate has diminished with the use of surfactants, the proportion ofsurviving infants with severe sequelae, such as chronic lung disease, cognitive delays, cerebralpalsy, and neurosensory deficits (i.e., deafness and blindness), has not. Although improvedneurodevelopmental outcomes have been reported in a few small studies, such improvement hasnot been seen on a global scale.

A study by the Eunice Kennedy Shriver National Institute of Child Health and HumanDevelopment (NICHD) Neonatal Research Network was undertaken to relate other known riskfactors with the likelihood of survival and impairment.[2] The study reported that 83% of infantsborn at 22-25 weeks' gestation received intensive care (consisting of mechanical ventilation). Ofall study infants whose outcomes were known at 18-22 months, 49% died, 61% died or had

profound impairment, and 73% died or had impairment.The report suggested the following 4 factors should be considered in addition to gestational agewhen determining the likelihood of favorable outcome with intensive care:

Sex - Female sex has the more favorable outcome Exposure to antenatal corticosteroids (with favorable effect) Single or multiple birth - Single birth has a favorable effect Birth weight - Increasing increments of 100g each add to favorable outcome potential


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According to data from a 2011 cohort study, infants born at born at 23-25 weeks' gestation whoreceived antenatal exposure to corticosteroids realized a lower rate of mortality andcomplications compared with those who did not.[3]

A meta-analysis by Laswell et al indicated that very low birth weight (VLBW) infants and verypreterm infants have increased odds of death when not born in level III hospitals.[4] In addition,

morbidity increases when the birth of these infants is not in a level III hospital, as the rates ofsignificant intraventricular hemorrhage (IVH) and periventricular leukomalacia (PVL), which areassociated with less than optimal neurodevelopmental outcome, also increase.

A study of 1064 infantsborn at 28 weeks gestation or less found that unless it is accompanied orfollowed by a white matter lesion, intraventricular hemorrhage was associated with a modest,and possibly no, increased risk of adverse developmental outcome during infancy (age 24mo).[5]

In a longitudinal study of 1279 extremely premature children (gestational age 28 wk; birthweight < 1250g), Robertson et al found permanent hearing loss in 3.1% and severe to profoundloss in 1.9%.[6] Among affected children, hearing loss was delayed in onset in 10% of them andwas progressive in 28%. Prolonged supplemental oxygen use was the most important marker for

predicting hearing loss.

One study evaluated the 11-year outcomes in 247 infants born in Sweden at less than 26 weeks'gestation between 1990 and 1992 and found that in infants who survive to a postmenstrual age of36 weeks, brain injury and severe retinopathy of prematurity (ROP), but not bronchopulmonarydysplasia (BPD), may predict the risk of death or major disability at age 11 years.[7]

Thermoregulation

As a result of a high body surface areatobody weight ratio, decreased brown fat stores,nonkeratinized skin, and decreased glycogen supply, infants with extremely low birth weight(ELBW) are particularly susceptible to heat loss immediately after birth. Hypothermia may resultinhypoglycemia,apnea, and metabolic.

Heat loss can occur in infants with extremely low birth weight in following 4 ways:

Conduction - The transfer of energy from the molecules of a body to the molecules of a solidobject in contact with the body, resulting in heat loss

Convection - The similar loss of thermal energy to an adjacent gas Evaporation - Evaporative heat loss is the total heat transfer by energy-carrying water

molecules from the skin and respiratory tract to the drier environment Radiation - Radiant loss is the net rate of heat loss from the body to environmental surfaces not

in contact with the bodyExtremely preterm infants are especially prone to these losses secondary to the poor barrierprovided by their thin, poorly keratinized skin.

Temperature control is paramount to survival and is typically achieved with use of radiantwarmers or double-walled incubators. Hypothermia (< 35C) has been associated with pooroutcome, including chronic oxygen dependency. Immediately after birth, the infant should bedried and placed on a radiant warmer and a hat or another covering should be placed on his orher head. Studies have shown that placing a plastic film over the baby immediately after dryingcan further minimize evaporative and convective heat losses.
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For transport to the neonatal intensive care unit (NICU) from the delivery room, the infantshould be covered with either warmed blankets or cellophane wrap. To transport the infant otherthan very short distances, he or she should be placed in a double-walled, heated incubator.

The delivery room and NICU should be kept warm to aid in the prevention of hypothermia in thepreterm infant. Architectural designs should facilitate adjacent location of delivery rooms and

NICUs or at least provide separately heated resuscitation rooms. Although chemical heating padsare commonly used to provide a warm surface on which to place the baby, the unregulated heatsource may burn the very fragile skin of the infant, so such pads are not recommended.[8]

Hypoglycemia

Fetal euglycemia (maintenance of normal blood glucose levels) is maintained during pregnancyby the mother via the placenta. Infants with extremely low birth weight (ELBW) have difficultymaintaining glucose levels within the reference range after birth, when the maternal source ofglucose has been lost. In addition, these infants are usually under increased stress compared withtheir term counterparts and have insufficient levels of glycogen stores. Preterm infants aregenerally considered hypoglycemic whenplasma glucose levels are lower than 45mg/dL.

Because symptoms of hypoglycemia (seizures, jitteriness, lethargy, apnea, poor feeding) may beless obvious in preterm infants, hypoglycemia may be detected only on routine sampling.

One form of accepted treatment consists of an immediate intravenous (IV) dextrose infusion of2mL/kg of 10% dextrose-in-water solution (200mg/kg), followed by a continuous IV infusion ofdextrose at 6-8mg/kg/min to maintain a constant supply of glucose for metabolic needs and toavoid further hypoglycemia.

Rapid infusion of glucose concentrations of greater than 10% should be avoided because of thehyperosmolarity of the solution and the risk of cerebral hemorrhage. Increased insulin secretionthat leads to a "rebound" hypoglycemia is a concern when the insulin is administered through anumbilical artery catheter.

Fluids and Electrolytes

Maintenance offluid and electrolyte balance is essential for normal organ function. Disturbancesmay result in or exacerbate morbidities, such aspatent ductus arteriosus (PDA),intraventricularhemorrhage (IVH), and chronic lung disease, which are also known asbronchopulmonarydysplasia (BPD).

Compared with full-term newborns, infants with extremely low birth weight (ELBW) haveproportionally more fluid in the extracellular fluid compartment than the intracellularcompartment, and a larger proportion of their body weight is attributable to water. During thefirst days after birth, diuresis may result in a 10-20% weight loss, which can be exacerbated byiatrogenic causes (e.g., radiant warmers, phototherapy).

These infants also have compromised renal function stemming from a decreased glomerularfiltration rate and a decreased ability to reabsorb bicarbonate. Immature renal tubular functionresults in decreased ability to secrete potassium and other ions with a relative inability toconcentrate urine. In addition, they reabsorb creatinine via the tubules following birth;thus,serum creatinine levels are elevated for at least the first 48 hours of life and do not reflectrenal function for the first few days following birth.
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Fluid status is commonly monitored with daily (or sometimes twice daily) body weightmeasurement, strict recording of fluid intake and output and frequent monitoring of electrolytes.

These infants are prone to nonoligurichyperkalemia,defined as aserum potassium level greaterthan 6.5mmol/L, which has been associated with cardiac arrhythmias and death.

Hypernatremia and hyponatremiaHypernatremia andhyponatremia, reflecting disturbances of free water relative to total bodysodium, are often disorders of water rather than sodium. As an infant with extremely low birthweight is exposed to radiant heat, phototherapy, and the relatively dry environment, substantialamounts of free water may be lost, causing a relative increase in sodium concentrations.

Management of hypernatremia in these infants consists of administration of hypotonic fluid toreplace the free water loss, perhaps requiring as much as 200-250mL/kg/day to maintainadequate hydration. Such large amounts of fluid can potentiate a PDA. However, free waterlosses may be decreased by early use of double-walled incubators.

On the other hand, hyponatremia in the first few days of life may be due to excess free water that

results in a dilutional hyponatremia, and restriction of fluid and sodium supplementation may bethe appropriate treatment.

Nutrition

Initiating and maintaining the growth infants with extremely low birth weight (ELBW) is acontinuing challenge. Infants are commonly weighed daily, and body length and headcircumference are usually measured weekly to track growth. The growth rate often lags becauseof complications such as pulmonary disease and sepsis.

An additional contributing factor is inadequate caloric and protein intake. Concern that earlyfeeding may be a risk factor fornecrotizing enterocolitis (NEC) often defers initiation of enteralfeeding, although nutritional management of such infants is marked by a lack of uniformity of

practice.

Parenteral nutrition

Parenteral nutrition may provide the primary source of energy and protein in infants withextremely low birth weight in the first few weeks after birth. Optimal parenteral nutrition isachieved by use of a specialized solution consisting of amino acids, dextrose (sugar), minerals,and electrolytes, called total parenteral nutrition (TPN). A 20% lipid emulsion is often runseparately to complete the nutrition of the infant. Lipid intake may vary from 1-4g/kg/day (astolerated) and should be started in the first 24 hours of life for optimal nutrition.

Theoretical concerns regarding infection and hyperbilirubinemia frequently lead to a delay in theinitiation of lipid supplementation.

Because these infants lose at least 1.2g/kg/day of endogenous protein, they require at least thatamount of amino acid and 30kcal/kg/day to maintain protein homeostasis. Recommendationsadvocate for initiation of protein supplementation within the first 12-24 hours to avoid proteincatabolism.

Some investigators postulate that total daily need to approximate fetal protein accretion rates inthese infants may be as high as 4g/kg/day. Evidence to date suggests that early and higher aminoacid provision is well tolerated by most infants with extremely low birth weight. Such provision
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of amino acids will positively affect the plasma amino acid concentrations during the firstpostnatal week but does not necessarily translate into a significant difference in postnatal growthin the first 28 days.[9, 10]

These infants also need essential amino acids, such as cysteine, and may require glutamine,found in human breast milk but not always present in parenteral nutrition mixtures.

Trace minerals, such as iron, iodine, zinc, copper, selenium, and fluorine, are beneficial as well.Early evidence suggests that chromium, molybdenum, manganese, and cobalt may need to beadded to the nutritional regimen, especially in infants who require long-term parenteral nutrition.Some centers also add L-carnitine.

Prolonged use of parenteral nutrition may result incholestasis and elevated triglyceride levels.To reduce these complications, regular laboratory tests are usually obtained to evaluate liverfunction, alkaline phosphates levels, and triglyceride levels.

Enteral nutrition

Enteral feeding is often begun when the infant is medically stable, using small-volume trophic

feeding (approximately 10mL/kg/day) to stimulate the gastrointestinal (GI) tract and preventmucosal atrophy. Bolus feedings every 2-4 hours may begin as early as day 1. If tolerated, asevidenced by minimal gastric residuals and clinical stability, feeding may increase by as much as10-20mL/kg/day, although feeding practices widely vary. Although bolus feeding may appear tobe more physiologically appropriate, infants who do not tolerate the volume of the bolus may becontinuously fed.

Clinical studies have consistently demonstrated that infants who are fed earlier and are advancedaccording to a feeding plan have less incidence of infection and achieve full enteral feeds soonerthan counterparts who are less systematically treated. Although the fear of precipitatingnecrotizing enterocolitis (NEC) remains widespread, randomized, controlled trials haverepeatedly failed to show any relationship between feeding practices (i.e., age at initiation,rapidity of advancement, caloric density) and the occurrence of NEC.

Breast milk is considered to be the best choice for enteral feeding and has been shown to haveprotective effects against NEC. Infants with low birth weight have a high need formacronutrients and micronutrients that approaches intrauterine needs; at the same time, theirfunctionally immature GI tract precludes adequate enteral intake.

Despite its many immunologic and nutritional advantages, an exclusive diet of unfortified breastmilk may provide insufficient quantities of energy, protein, calcium, and phosphorous to supportthe goals of intrauterine bone mineralization and growth rates in small, premature infants.Consequently, breast milk must be fortified to provide additional calories, protein, and mineralsto promote proper growth. Failure to provide adequate amounts of these essential nutrients,

especially calcium and phosphorus, may result in protein malnutrition, hyponatremia, osteopeniaof prematurity, or rickets.

Human milk may be supplemented by adding liquid or powder commercially available fortifiers,premature infant formulas, modular supplements, or vitamin/mineral supplements. Commerciallyavailable multinutrient fortifiers include Enfamil Human Milk Fortifier (Mead JohnsonNutritionals; Evansville, Indiana) or Similac Human Milk Fortifier (Ross Products, AbbottLaboratories; Columbus, Ohio), both of which are powders. The 2 formulations have some


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significant differences in their compositions, which may be clinically important. Similac NaturalCare Liquid Fortifier (Ross Products) is also available.

Comparisons of the nutrient content and source of macronutrients of these fortifiers have beenpublished. Potential complications of human milk fortifiers include nutrient imbalance, increasedosmolarity, and bacterial contamination. Numerous specially formulated preterm formulas are

available that have been shown to promote proper growth when breast milk is not available.

Balance of nutrients is very important in early nutrition. Studies suggest that a high carbohydrateneonatal diet is linked to greater weight gain and reduced insulin sensitivity in extremely preterminfants, making them at risk for metabolic syndrome later in life.

Hyperbilirubinemia

Most infants with extremely low birth weight (ELBW) develop clinically significanthyperbilirubinemia (jaundice) that requires treatment. Hyperbilirubinemia develops as a result ofincreased red blood cell (RBC) turnover and destruction in the context of an immature liver thathas physiologically impaired conjugation and elimination of bilirubin. In addition, most preterminfants have reduced bowel motility due to inadequate oral intake, which delays elimination of

bilirubin-containing meconium, coupled with increased enterohepatic circulation of conjugatedbilirubin that enters the intestinal tract.

These complications of extreme prematurity, in addition to typical conditions that cause jaundice(e.g., ABO incompatibility, Rh disease, sepsis, inherited diseases), are thought to place theseinfants at higher risk forkernicterus at levels of bilirubin far below those in more mature infants,although specific serum bilirubin levels that are safe versus toxic have never been elucidated.

Kernicterus occurs when free, unconjugated bilirubin crosses the blood-brain barrier (BBB) andstains the basal ganglia, pons, and cerebellum; diminished protein status and the occurrence ofacidosis in infants with extremely low birth weight may potentiate the proportion of unboundbilirubin available to cross the BBB. Infants with kernicterus who do not die may have sequelae

such as deafness, mental retardation, and cerebral palsy.

Phototherapy

Phototherapy is used to decrease bilirubin levels to prevent the elevation of unconjugatedbilirubin to levels that cause kernicterus. Special blue-green lamps with wavelengths of 420-475nm are used to break down unconjugated bilirubin to the more water-soluble productlumirubin via photoisomerization and photo-oxidation through the skin. This product can then beeliminated in bile and urine.

The light source is positioned at 50cm above the infant, with the rate of bilirubin reduction beingdirectly proportional to the light intensity. Clinical studies have shown maximum effectivenesswhen the intensity of the light exceeds 12-15W/cm2.

Newer phototherapy lights have been developed that decrease the amount of insensible waterloss due to photo-induced vasodilatation. In extremely premature infants, insensible water losscan still be significant, and careful attention must be paid to fluid balance. As with the oldermodels, the infant's eyes should be covered with patches to avoid exposure to the blue light.White light phototherapy is not as effective. Fiberoptic blankets may be used, although skinburns from the devices are concerning.


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Although phototherapy of these infants is initiated at birth at some institutions, others startphototherapy when the bilirubin value approaches 50% of the birth weight value (eg, 4mg/dL inan 800g infant). Use of prophylactic phototherapy has not been shown to decrease the peak levelof totalserum bilirubin (TSB) or the duration of phototherapy.

Exchange transfusion

If the level of bilirubin does not satisfactorily decrease with phototherapy, exchange transfusionis the next therapeutic option. Exchange transfusion should be considered if the level of bilirubinapproaches 10mg/dL (or 10mg/dL/kg). In otherwise healthy term infants, exchange transfusion isnot considered until the bilirubin level approaches greater than 20-25mg/dL and the infant hasfailed a trial of phototherapy.

In exchange transfusions, almost 90% of the infant's blood is replaced with donor blood, and, ifcorrectly performed, the bilirubin level usually falls to 50-60% of the preexchange level.Complications of exchange transfusion include electrolyte abnormalities (e.g.,hypocalcemia,hyperkalemia), acidosis, thrombosis, sepsis, thrombocytopenia, and bleeding.

Respiratory Distress and Chronic Lung Disease

An early complication of extreme prematurity isrespiratory distress syndrome (RDS) caused bysurfactant deficiency. Clinical signs include tachypnea (>60 breaths/min), cyanosis, chestretractions, nasal flaring, and grunting. Untreated RDS results in increasing difficulty inbreathing and increasing oxygen requirement over the first 24-72 hours of life. Chestradiography reveals a uniform reticulogranular pattern with air bronchograms.

As a result of surfactant deficiency, the alveoli collapse, causing a worsening of atelectasis,edema, and decreased total lung capacity. Surfactants decrease the surface tension of the smallerairways so that the alveoli or the terminal air sacs do not collapse, which results in less need forsupplemental oxygen and ventilatory support.

The incidence of RDS is inversely proportional to gestational age, with an incidence of 60% at29 weeks' gestation. RDS affects about 40,000 infants in the United States annually (most infantswith extremely low birth weight [ELBW] are affected). Common complications include air leaksyndromes, chronic lung disease or bronchopulmonary dysplasia (BPD), andretinopathy ofprematurity (ROP).

Surfactant agents and antenatal steroids

Surfactant agents may be administered as prophylaxis or as rescue intervention after RDS.Prophylactic use in infants younger than 28 weeks' gestation has been shown to decrease short-term ventilatory needs; neither strategy has resulted in a decreased incidence of chronic lungdisease (BPD).

Synthetic surfactants currently on the market lack the proteins found in animal-derivedsurfactants and may not be as effective as the latter. Newer synthetic surfactants with a syntheticsurfactant protein analog are being tested.

The incidence of RDS in preterm infants has been significantly reduced with the use of antenatalsteroids to promote lung maturity; an additive effect was seen with the use of both antenatalsteroids and early surfactant treatment. The use of antenatal steroids also has been linked to areduction in the incidence of clinically significant patent ductus arteriosus (PDA) and severe
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intraventricular hemorrhage (IVH); however, concerns have surfaced regardingneurodevelopmental sequelae of repeated antenatal courses of steroids.

In the last decade, surfactants have been widely used to treat RDS, and it was suggested thatsurfactants should be routinely administered as prophylaxis in infants younger than 30 weeks'gestation. However, this results in unnecessary treatment in some infants. A shift in practice is

occurring, and fewer infants are immediately intubated after birth, making prophylactic treatmentwith surfactant impossible.

If used as prophylactic treatment, surfactants should be administered as soon after birth aspossible. When administered as rescue treatment, a reasonable approach is to treat most infantsas soon as clinical signs of RDS appear or if the respiratory picture does not improve after theinitial resuscitation.

Continuous positive airway pressure

Infants who are not immediately intubated are usually maintained with nasal continuous positiveairway pressure (CPAP), which has been shown to improve endogenous surfactant production.These infants are intubated and given surfactant only if they fail the initial trial of CPAP, asevidenced by increasing PaCO2, increasing respiratory distress, or persistently high oxygenrequirement.

A retrospective analysis studied the first 48 hours in 225 infants of 23-28 weeks' gestational ageand noted that 140 of these infants could be stabilized with nasal CPAP in the delivery room, 68with a favorable outcome and 72 with a failed outcome within 48 hours. History or initial bloodgas results were poor predictors of subsequent nasal CPAP failure. A threshold fraction ofinspired oxygen (FiO2) of greater than or equal to 0.35-0.45 compared with greater than or equalto 0.6 for intubation may shorten the time to surfactant delivery, without a relevant increase inintubation rate.[11]

A study by Geary et al was promising for a reported decrease in incidence of chronic lungdisease using this approach (along with lowered oxygen saturation limits and aggressive earlynutrition).[12]

Chronic lung disease

A major morbidity of premature birth is chronic lung disease (BPD), which is defined as a needfor supplemental oxygen or ventilatory support at 36 weeks' postmenstrual age. This definitionhas, to a relative extent, replaced the former definition of oxygen dependence beyond age 28days.

BPD is a staged disease that was originally described by Northway et al in 1967 as the clinicalsequelae of prolonged ventilation associated with radiographic and pathologic findings; it is the

result of abnormal reparative processes in response to injury and inflammation.[13]

The NICHD Neonatal Network reported that the incidence of BPD at 36 weeks in all infants whoweighed 501-1500g increased from 19% in 1990 to 23% in 1996.[14]This figure remained steadyat 22% in 2000. Sixty percent of very low birth weight infants requiring prolonged mechanicalventilation were oxygen dependent at age 28 days, and 30% remained oxygen dependent at 36weeks' postmenstrual age. For infants with extremely low birth weights, the overall incidence ofBPD was 40%, with as many as 77% of infants requiring mechanical ventilation developing thedisease. No further decrease in the incidence of BPD has been observed since 1996.


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Inhaled nitric oxide (iNO) has been used in attempts to either rescue extremely ill preterm infantsor to help prevent BPD.[15] As a rescue, this treatment is linked to an increase in severe IVH.Unfortunately, iNO is also relatively ineffective in preventing BPD. However, it may decreaseserious brain injury and improve rates of survival without BPD in mildly ill preterm infants whenconsistently used. Further studies are currently underway.

A study by Wilkinson et al reported changes in brainstem auditory evoked responses (BAER) ininfants with BPD.[16] Their results suggested that these infants had "poor myelination andsynaptic function of their brainstem, resulting in impaired functional integrity." Their peripheralneural function did not appear to be affected by their lung disease. Additional studies ofbrainstem function in infants with BPD are needed to further define what neurologicabnormality, if any, is present.

Patent Ductus Arteriosus

In the fetus, oxygenation of the blood is accomplished by the placenta, making blood flowthrough the lungs unnecessary. The ductus arteriosus is a conduit between the left pulmonaryartery and the aorta that results in shunting of blood away from the lungs while the infant is in

utero. In full-term newborns, the patent ductus arteriosus (PDA) typically closes within 48 hoursof birth because of oxygen-induced constriction.

However, the PDA in preterm infants is less responsive to this effect of oxygen, and as many as80% of infants with extremely low birth weight (ELBW) have a clinically significant PDA. Thisresults in a shunt from the systemic circulation into the pulmonary circulation (a so called left-to-right shunt) that causes various symptoms, including a loud systolic murmur, widened pulsepressures, bounding pulses, hyperactive precordium, and increased effort to breathe. Ahemodynamically significant PDA has a negative effect on cerebral oxygenation in the preterminfant.

Because of a net decrease in systemic cardiac output due to this left-to-right shunting, decreased

urine output, feeding intolerance, and hypotension may also occur.Treatment

The diagnosis of PDA is typically confirmed using echocardiography, and treatment includesdecrease of fluid intake, indomethacin or ibuprofen administration, and surgical ligation, ifnecessary. Adequate treatment of PDA has long been theorized to prevent diminished cerebralperfusion and subsequent decreased oxygen delivery. However, more recent studies havesuggested that aggressive treatment of PDA with surgical ligation may be associated with ahigher rate of chronic lung disease.[17]

Indomethacin is used prophylactically at some institutions and is administered in the first 24hours of life to close a PDA in anticipation of the deleterious effects of a continued PDA in an

infant with extremely low birth weight. Some evidence suggests that prophylactic use ofindomethacin has led to decreased symptomatic PDAs and PDA ligations in these infants.[18]

Concerns regarding indomethacin and its effects on cerebral and renal blood flow have led to theinvestigation of other drugs, such as IV ibuprofen, which is now available as an alternative agentto close PDAs in preterm infants. Use of ibuprofen in premature baboons for PDA closure wasshown to improve pulmonary mechanics, decrease total lung water, increase epithelial sodiumchannel expression, and decrease the detrimental effects of preterm birth on alveolarization in


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one study.[19] However, caution is recommended because the risks associated with indomethacinare also associated with ibuprofen.

Infection

Infection remains a major contributing factor to the morbidity and mortality of infants withextremely low birth weight (ELBW) and can present at any point in the clinical course. Early

onset infection (occurring within the first 72h of life) may present with immediate respiratorydistress shortly after birth or after an asymptomatic period.

No matter the timing of presentation, the sequence of events leading to early onset infectionbegins with colonization of the newborn with bacteria from the maternal genital tract. Herpesviral infection in the newborn is transmitted in a similar manner, but infants generally do notbecome symptomatic until after the first week of life. Late infections typically occur after thefirst week of life and result from endogenous hospital flora (nosocomial).

Signs of infection are myriad and may be nonspecific; they include the following:

Temperature instability - Hypothermia or hyperthermia

Tachycardia Decreased activity Poor perfusion Apnea Bradycardia Feeding intolerance Increased need for oxygen or higher ventilatory settings Metabolic acidosis

Laboratory studies may include complete blood count (CBC) with differential,blood culture,cerebrospinal fluid culture,urine culture, and cultures from indwelling foreign bodies, such ascentral lines or endotracheal tubes.

Causes

The most common causes of early sepsis in the immediate newborn period are group Bstreptococci (GBS) andEscherichia coli. Nosocomial sources of infection include coagulase-negative staphylococci (CoNS) andKlebsiellaandPseudomonasspecies, which may be resistantto the antibiotics typically started for early onset sepsis, necessitating a different treatmentregimen. Methicillin-resistant Staphylococcus aureusis also becoming more common.

Fungi, most commonly Candida albicans,are frequently a cause of late-onset sepsis in infantswith extremely low birth weight and may manifest with the above-mentioned symptoms andthrombocytopenia, particularly if the infant has been exposed to broad-spectrum antibiotics.

Indolent late-onset sepsis may be related to CoNS, while fulminant late-onset clinical sepsis ismore commonly secondary to gram-negative organisms. Late-onset sepsis is especially commonin infants with extremely low birth weights who have indwelling catheters and may occur in asmany as 40% of these infants.

Treatment

In most institutions, first-line therapy in infants with early sepsis is with ampicillin andgentamicin or a third-generation cephalosporin. Vancomycin should be reserved for proven
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diagnoses for NEC include benign feeding intolerance, septic ileus, inspissated meconiumsyndrome, Hirschsprung enterocolitis, and severegastroenteritis.

Intraventricular Hemorrhage

A hemorrhage in the brain that begins in the periventricular subependymal germinal matrix canprogress into the ventricular system, causing intraventricular hemorrhage (IVH). The incidence

and severity of IVH are inversely related to gestational age.

Babies with extremely low birth weight (ELBW) are at particular risk for IVH because ofvulnerability of the germinal matrix and because the protective cerebral autoregulation present inolder babies has not yet developed. Any event that results in disruption of vascularautoregulation can cause IVH, including hypoxia, ischemia, rapid fluid changes,andpneumothorax.

Presentation can be asymptomatic or catastrophic, depending on the degree of the hemorrhage.Symptoms include the following:

Apnea

Hypertension or hypotension Sudden anemia Acidosis Changes in muscular tone Seizures

The most commonly used classification system divides IVH into 4 grades, as follows:

Grade I - Germinal matrix hemorrhage Grade II - IVH without ventricular dilatation Grade III - IVH with ventricular dilatation Grade IV - IVH with extension into the parenchyma

Diagnosis and treatment

IVH is diagnosed using cranial ultrasonography. Because most IVHs occur within 72 hours ofdelivery, neurosonography is usually performed on infants with extremely low birth weightduring the first week after birth and serially thereafter, depending on clinical scenario. The use ofantenatal steroids decreases the incidence of IVH, and treatment consists of supportive care.

Progressive intraventricular dilatation and hydrocephalus may necessitate surgical diversion ofaccumulating cerebrospinal fluid. Early administration of indomethacin may reduce theincidence of grades III and IV IVH when used prophylactically in infants with extremely lowbirth weight but may adversely affect urine output and platelet function and has not been shownto improve neurodevelopmental function at age 2 years.

Prognosis is correlated with the grade of IVH. The outcome in infants with grades I and II isgood, but these infants require close neurodevelopmental follow-up because, in a study byVasileiadis et al, uncomplicated IVH was associated with impaired cortical development (asevidenced by reduced cortical volume at near-term age).[20]

As many as 40% of infants with grade III IVH have significant cognitive impairment, and asmany as 90% of infants with grade IV IVH have major neurologic sequelae, requiring lifetimecare.
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Prevention of preterm birth is the most effective method of preventing IVH. The risk of IVH ishigher in infants who are transported after birth, underlining the need for preterm births to occurat tertiary centers specializing in high-risk deliveries. Adequate resuscitation is paramount, andhypocarbia and hypoxia should be avoided. Maintenance of adequate mean arterial pressure andavoiding elevations in cerebral blood flow as much as possible are vital.

Multiple clinical trials have been undertaken to determine the effect of various medications,either antenatally or perinatally, on the incidence of IVH. One trial demonstrated a decrease inthe incidence of severe grades of IVH but no difference in neurodevelopmental outcomes at age18-24 months with the use of postnatal indomethacin. Because of the potentially seriouscomplications of indomethacin, the question of using such an approach remains unanswered.

Periventricular Leukomalacia

Periventricular leukomalacia (PVL) is defined as damage to cerebral white matter that can resultin severe motor and cognitive deficits in infants with extremely low birth weight (ELBW) whosurvive; it occurs in 10-15% of these infants. PVL most often occurs at the site of the occipitalradiation at the trigone of the lateral ventricles and around the foramen of Monro.

The origin of PVL is believed to be multifactorial; the injury possibly results from episodes offluctuating cerebral blood flow, which are caused by prolonged episodes of systemichypertension or hypotension. PVL has also been linked to periods of hypocarbic alkalosis andchorioamnionitis.

PVL may be diagnosed using brain ultrasonography in patients aged 4-6 weeks, with magneticresonance imaging (MRI) providing the definitive diagnosis. Terminology to characterizevarious patterns of white matter injury is currently in a state of flux, reflecting differentpathophysiologic mechanisms thought to underlie the observed abnormalities. The presence ofPVL, particularly cystic PVL, is associated with an increased risk of cerebral palsy; spasticdiplegia is the most common outcome.

With the current ability to use MRI for evaluation of the brain prior to discharge, the incidence ofdiagnosed PVL and other intracranial pathologies can be expected to increase.

Apnea of Prematurity

Apnea of prematurity (AOP), which is common in infants with extremely low birth weight(ELBW), is defined as cessation of respiratory activity of more than 20 seconds, with or withoutbradycardia or cyanosis. These episodes are usually random and may be difficult to distinguishfrom the gestationally normal pattern of periodic breathing demonstrated in this age group.Apneic episodes are considered clinically significant if they are greater than 20 seconds induration and/or are accompanied by bradycardia or change in color or oxygenation. Theincidence of AOP is inversely correlated with gestational age and weight, occurring in as many

as 90% of infants who weigh less than 1000g at birth.Causes

Apnea can be caused by decreased central respiratory drive, which causes what is termed centralapnea, or by an obstruction in which no nasal airflow occurs despite initiation of respiration(obstructive apnea). AOP in a pure sense is secondary to immature respiratory patterns and maybe due to a combination of central and obstructive apnea (mixed apnea), in which a lack ofcentral respiratory stimulation is followed by airway obstruction.
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Episodes of apnea may also be induced by hypoxia, sepsis, hypoglycemia, neurologic lesions,seizures, and temperature irregularities. Apnea is clinically diagnosed and can be detected viause of cardiorespiratory monitors and pulse oximetry. Pneumography can be used to illustrate thenumber and severity of the apneic episodes, with or without bradycardia, in conjunction with acontinuous electrocardiography recording.

Treatment and monitoring

Treatment of AOP includes nasal continuous positive airway pressure (CPAP) and use ofpharmacologic agents, such as theophylline and caffeine. Caffeine appears to be more effectivein stimulating the CNS and has a wider therapeutic range, while causing less tachycardia thantheophylline. Theophylline is more efficacious than caffeine as a bronchodilator and diuretic andis often used as an adjunct therapy for bronchopulmonary dysplasia (BPD).

Studies of long-term effects of caffeine on neonatal outcomes are currently underway by theCaffeine for Apnea of Prematurity Trial Group, and thus far, no long-term ill effects have beennoted. The incidence of BPD was decreased at hospital discharge for those infants who receivedcaffeine therapy for AOP, and follow-up studies (age 18-21mo) suggested a decrease in

neurodevelopmental disability.[21] Follow-up at 5 years is the next goal of this group.

Premature infants who are believed to have AOP at the time of discharge may be sent home withan apnea monitor, although the use of home apnea monitors in infants with AOP remainscontroversial. AOP often persists beyond 40 weeks' corrected age, which is longer than waspreviously believed, although most cases completely resolve by 43 weeks' postmenstrual age. Noassociation between AOP andsudden infant death syndrome (SIDS) has been proven, and theuse of home apnea monitoring has not been shown to decrease the incidence of infant deathsecondary to SIDS. Home apnea monitoring requires training of caregivers in the use of themonitor and in cardiopulmonary resuscitation for infants.

Anemia

Physiologic anemia, also seen in term infants, occurs earlier and is more profound in preterminfants. Multiple reasons for this increased severity of anemia have been proposed, includingphysiologic responses to decreased oxygen consumption (compared with term), blood losssecondary to phlebotomy for laboratory studies related to clinical management in the first fewweeks of life, a developmentally immature erythropoietic response to anemia, decreased survivalof RBCs in preterm infants, and deficiencies of folate, vitamin B-12, or vitamin E.

Treatment of anemia in premature infants includes transfusion with packed RBCs (PRBCs).Administration of recombinant human erythropoietin and iron to increase erythropoiesis has notbeen shown to prevent the need for transfusion in the first few weeks of life. Most transfusionsoccur in the first few weeks of life to help replace losses secondary to phlebotomy; infants withextremely low birth weight (ELBW) usually receive at least 1 transfusion at some point duringthe neonatal stay. Transfusions occurring after the first weeks of life are usually in response tosigns and symptoms of severe anemia.

To reduce the risk of infection in preterm neonates, infants are often assigned a "dedicated unit"from which they can receive multiple transfusions until the unit expires. In addition, manyNICUs have adopted a policy of minimal blood draws and strict transfusion guidelines tominimize the need for transfusion. Arbitrary threshold hematocrits that trigger transfusion arebeing replaced clinically by delay until the infant develops adverse symptoms from the anemia.


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Anecdotal reports of necrotizing enterocolitis (NEC) occurring within 48 hours after transfusionin asymptomatic, growing premature infants has served to further discourage the practice ofroutine transfusion.

Immunization of Preterm Infants

Preterm infants are at high risk for increased morbidity from vaccine-preventable diseases but

are the most likely group to have delayed immunizations. Many parents, as well as somephysicians, regard preterm infants as frail and tenuous, even if they are relatively stable. TheAmerican Academy of Pediatrics (AAP) policy states that preterm infants should receive fulldoses of diphtheria, tetanus, acellular pertussis,Haemophilus influenzaetype b, poliovirus, andpneumococcal conjugate vaccines at the appropriate chronologic age.[22] Hepatitis B vaccine isrecommended by the age 30 days and may be given at birth or at age 1 month, as per individualunit policies.

Some studies have suggested that immunologic response to hepatitis B vaccine is improved if theinfant is more than 2000g at the time of administration, but the AAP does not recommenddelaying this immunization beyond 30 days of age. As always, infants of mothers with serology

positive for hepatitis B surface antigen should receive the vaccine shortly after birth, along withhepatitis B immunoglobulin (HBIG). Guidelines for administration in premature infants whosematernal status is unknown recommend HBIG/hepatitis B vaccine within the first 12 hours of life

Emotional Reaction of Parents

The birth of an extremely premature infant or an infant with an extremely low birth weight(ELBW) is associated with a unique kind of stress to a family dynamic. Parents of such an infantoften experience wide swings of emotion as their child's time in the care of the NICU progresses.They also often experience all 5 stages of grief, from denial to acceptance.

In addition, the strain on the marriage relationship caused by the birth of an extremely prematureor extremely low birth weight infant can be tremendous and may result in divorce if not

anticipated early in the course of the infant's life. Great care must be taken by caregivers to beconsiderate of the myriad emotions experienced by parents while care is given to their infant;these caregivers should be prepared to provide additional support to the family.

Follow-Up Care

Neurodevelopment

Nearly all infants with extremely low birth weight (ELBW) require neurodevelopmental follow-up monitoring to track their progress and to identify disorders that were not apparent during thehospital stay. These infants typically have complicated medical courses and often go home withmultiple treatments and medications. The goals of the neonatal follow-up clinic are as follows:

Early identification of developmental disability Parental counseling Identification and treatment of medical complications Provision of feedback for neonatologists, pediatricians, obstetricians, and other providers

Specific evaluations of cognitive development, vision and hearing ability, andneurodevelopmental progress is extremely important.

Most preterm infants are not significantly handicapped, but this group of infants does have ahigher incidence of cerebral palsy and mental retardation than does the general


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population.[23] They also have a higher risk of disorders of higher cognitive function, such aslanguage disorders, visual perception problems, attention deficits, and learning disabilities.

Infants with grades III or IV intraventricular hemorrhage (IVH) or infants with periventricularleukomalacia (PVL), which are cysts in brain parenchyma that are typically seen on routine brainultrasonography in infants aged 4-6 weeks, are at the greatest risk for mental retardation. Other

risk factors for developmental disabilities include maternal chorioamnionitis, meningitis, sepsis,asphyxia, delayed head growth, and chronic lung disease.

Marlow et al published a follow-up of the EPICure study in which they found that infants bornbefore 26 weeks' gestation had significant cognitive and neurologic impairment at schoolage.[24] The unique design of this study included comparing these children with their school-agedpeers. In the report, which was conducted in the United Kingdom and Ireland, 241 patients werecompared with 160 classmates born at full term.

Marlow and colleagues also found that 38% of those infants who showed no disability or milddisability at 30 months progressed to moderate to severe disability by school age. These childrenmay not have been classified as severe had they been measured on traditional scales rather than

being compared with their healthy peers; this sheds new light on the true incidence of disabilityin extremely preterm infants.

A study of Australian-born very preterm infants with extremely low birth weight, published in2003 by Anderson and colleagues, found that survivors who were followed until age 8 years hadintelligence quotient (IQ) scores in the average range but that the mean values were lower thanvalues seen in normal birth weight controls.[25]

The parents of the followed infants also reported more behavioral issues than did those withinfants who had a normal birth weight. These children also had significantly slower educationalprogress than their normal birth weight peers, although their formal scores on academicachievement tests for reading and spelling were within the average range.

According to the teachers involved with these students, members of the very preterm cohort werelagging in the areas of verbal thinking, speech, reading, writing, handwriting, mathematics,general facts, basic motor generalizations, and social behavior. These differences were still seenwhen children with neurosensory deficits were excluded and adjustment was made forsociodemographic variables.

In a study of 148 ELBW children, Voss et al found that maternal educational background wasthe strongest predictor of long-term neurodevelopment, pointing to the need for follow-up careand support for poorly educated parents.[26]

The data from a study of low birth weight twins found evidence of a causal association betweenbirth weight and attention problems. In birth-weightdiscordant monozygotic (MZ), dizygotic

(DZ), and unrelated (UR) pairs, the child with a lower birth weight (1500-2000g) scored higheron tests for hyperactivity and attention problems than did the child with a higher birth weight(3000-3500g). Within-pair differences were similar for MZ, DZ, and UR pairs.[27]

Vision

In the disorder retinopathy of prematurity (ROP), the premature retina has not yet fullyvascularized. Changes in oxygen exposure have been postulated to cause a disruption in the


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natural course of vascularization and may result in abnormal growth of blood vessels, which canlead to retinal detachment and blindness.

Risk factors for severe ROP include prematurity and exposure to oxygen. The number ofnewborns cared for by a nurse is likely a significant factor that contributes to the precision ofaccomplishing targeted oxygen-saturation goals in the NICU. The precision and the mode of

assisted ventilation may be modifiable factors worthy of attention in the NICU as effortscontinue to be made to reduce ROP and other oxygen-related toxicities.[28]

All infants with extremely low birth weight should undergo an eye examination by anexperienced pediatric ophthalmologist at chronologic age 4 weeks (or at 31 weeks'postconceptual age if the infant was born prior to 27 weeks' gestation) and, depending on theresults, at least every 2 weeks thereafter until the retina is fully vascularized, even if the infant isdischarged from the NICU.

If ROP is present, its stage and location dictate management, which can range from frequentrepeat examinations to laser surgery or even vitrectomy. The presence of significant plus disease,or tortuosity, of the retinal vessels, is a poor prognostic sign and requires immediate treatment.

Infants with ROP are also at greater risk for sequelae, such as myopia, strabismus, andamblyopia.

Infants with extremely low birth weight who do not have ROP or who have resolved ROP shouldhave a follow-up eye examination at age 6 months.

A study of the effects of human milk on the development of ROP failed to yield the hoped-forresult; the report found that consuming human milk did not reduce the risk of severe ROP ininfants with extremely low birth weight.[29]

Hearing

All infants should undergo hearing examinations prior to discharge, using either evoked

otoacoustic emissions or brainstem auditory evoked potentials. Infants with extremely low birthweight are at higher risk for hearing impairment because of their low birth weight. Other riskfactors include meningitis, asphyxia, exchange transfusions, and administration of ototoxicdrugs, such as gentamicin. These infants should have a repeat hearing examination at age 6months.

Intervention programs

All infants with extremely low birth weight should be referred to their local early interventionprogram or something similar. These programs allow for physical, occupational, and speechtherapy evaluations and provide in-home treatment. In the United States, these programs areavailable in all states and in most counties.

These programs should be coordinated with the infant's pediatrician and with the follow-up careclinic. As an increasing number of babies are born and continue to survive with a birth weight ofless than 1000g, optimizing their chances for a healthy, productive life is important.

Ethical, Economic, and Legal Considerations

Questions regarding ethical, economic, and legal considerations surrounding the care of infantswith extremely low birth weight (ELBW) continue to grow as the number of infants with this


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condition continues to increase in the postsurfactant era. Moreover, the United States is no longeralone in confronting neonatal-perinatal medical, legal, and ethical issues.

The physician must recognize that decisions concerning these issues are influenced by his or herown views of what is beneficial and just and must learn to see these issues from all points ofview (ie, the parents', siblings', extended family's, infant's, and society's as a whole). In this

situation, the clinician has 3 ethical obligations: (1) to understand his or her own value system;(2) to possess some knowledge of ethics as a formal discipline; and (3) to make the actualclinical decision and implement it in a morally defensible way.

Management of anticipated delivery of an infant with extremely low birth weight and subsequentcare requires the clinician to make decisions "in the moment of clinical truth." As informationregarding mortality, morbidity, and prognosis changes with time, clinicians must make thedecisions they feel to be right for the patient and the family at the time. Using the bestinformation available, the clinician should manage the situation while taking into account thefamily's wishes and what is in the best interests of the infant and the mother.

When resolving bioethical dilemmas facing families and clinicians, the physician must address

issues of futility, extension of the dying process, respect for the dignity of life, and pain andsuffering. From a legal standpoint in the United States, government regulations are based onchild abuse laws and are enforced by individual states.

The question of what to do in the case of extreme prematurity (23 weeks' gestation) is a

difficult one. Gestational age, which is typically based on the mother's recount of her lastmenstrual period, can differ from the actual gestational age by as much as 2 weeks, even whenthe latest ultrasonographic technology is used. Most centers do not have minimum birth weightcriteria for resuscitation, and often a "trial of life" may be discussed with the parents before thebirth so that the infant can be resuscitated and evaluated for viability after birth.

Viability

Viability is the term frequently used to indicate the possibility for a fetus to be live born andcapable of surviving to a specified endpoint (ie, a designated time, reaching a certain age andlandmark event, admission to the NICU, or discharge from the hospital).

Many institutions have generated center-specific data to help discuss the probability of survivalwith families prior to delivery. In this instance, care must be taken to explain that the fetus inquestion could actually be part of the percentage of nonsurvivors and that survival may comewith varied disabilities. Discussions about treatment or withdrawal of support are often necessarywhen the family and medical team agree that continuation of medical treatment is not in theinfant's best interests.

Naturally, these circumstances raise numerous ethical, moral, and legal issues and sometimes

generate more questions than answers. Bioethics consultants and multidisciplinary ethicscommittees often discuss such issues in an attempt to arrive at recommendations for cliniciansand families. Pellegrino outlined the following 5-step schema for arriving at such decisions[30] :

Establish the facts Determine what is in the patient's best interests Define the ethical issues and principles State the decision in concrete terms


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Justify the decisionEach of these steps can be a difficult process that yields new insights into the family's andpatient's needs, as well as into the clinician's biases.

Costs

In 2003, researchers from Helsinki published data on the costs of care for infants with extremelylow birth weight during the first 2 years of life.[31] They studied 71 infants with extremely lowbirth weight and compared them with 60 infants with normal birth weight born in their hospitalfrom 1996-1997. Taking into account costs of hospitalization, outpatient care, medication,rehabilitation and travel, ancillary costs from daily care, cost of parents' accommodation duringhospitalization periods, and loss of earnings until the corrected age of 2 years, they calculated thetotal healthcare cost for surviving infants with extremely low birth weight to be 104,635 euros(approximately $125,562 US dollars).

The average cost for a healthy, term control infant was 3,135 euros (approximately $3,762 USdollars), with an average of 19,950 euros (approximately $23,940 US) for nonsurviving infants.Breaking down these costs, a normally developed infant with extremely low birth weight had a

25-fold increase in costs over the term controls, whereas mild disability resulted in a 33-foldincrease, and severe disability resulted in a 68-fold increase.

In the United States, one must consider the higher overall health care costs and the fact that paidmaternity leave is usually 6 weeks or less, resulting in a larger proportion of lost wagessecondary to the birth of an infant with extremely low birth weight. Such factors make thesefigures significantly higher.

An article published in 2007 inPediatrics suggested the hospitalization costs for preterm andlow birth weight admissions in 2001 totaled $5.8 billion.[32] The average cost for an infant born atless than 28 weeks' gestation or less than 1000g birth weight in this study was $65,600, thehighest of all groups studied.

As technology advances, health care costs will continue to rise; the care team must take intoaccount the severe emotional and financial stress encountered with the birth of an infant withextremely low birth weight. The family is often confused, angry, and frustrated by resultingissues. In addition, society in general is affected by these infants, many of whom have significantcognitive or physical impairment and require lifelong public assistance.

Considerations pending and after delivery

Although addressed by revisions in the World Health Organization (WHO)/American HeartAssociation (AHA)/American Academy of Pediatrics (AAP)endorsed Neonatal ResuscitationProgram (NRP) protocol, no single rule has been written regarding what to do in the impendingbirth of an extremely premature infant.

The obstetrician and the neonatologist must talk with the parents regarding what can be expectedafter delivery. The role of the medical team is (1) to fully inform the parents, based on theexpected gestational age and any other pertinent prenatal data, of the most recent local andnational statistics describing morbidity and mortality; (2) to describe procedures that may occurafter the infant is delivered; and (3) to answer any questions the parents may have regarding theirinfant's care.


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Remember that opportunities to discuss management options are available after the infant isborn, allowing better evaluation of the infant and time for the family to fully comprehend thesituation. Documentation by the clinician of these encounters helps to guide further decisions inthe care of the infant and guard against future liability.

Documents

Extremely Low Birth Weight Gopal