TM5559: Clinical Tropical Paediatrics

Case Study Two: A case of prematurity and intrauterine growth restriction. Samantha Leggett: SN 12494652

8/2/2011

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Case Study Two

A case of prematurity and Intrauterine Growth Restriction

Female Infant (FI) of AA

DOB: 15-10-2010

Gestation: Thought to be 31 weeks

Birth Weight 1000g

Sociodemographic Details: Family live in Uia Village, Bugati, Madang (approx 1 ½ hours from Madang, 4 Kina/ $1.60 on PMV). Baby is child number seven and Mum (AA) reports that all other children are healthy and that the eldest two are at school. Mum and Dad are both alive and are married and living together. Mum reports that neither she nor her husband has received any education. Neither is formally employed but they have a small market garden which they make a little money from.

Background: Baby’s mother presented to Modilon General Hospital (MGH) on 15-10-10 with a history of 8 hours of labour pains. She had had 3 ante natal visits early in her third trimester and had been advised to make her way to MGH if labour started as she was considered a high risk pregnancy1.

Findings at Birth: Baby was born by standard vaginal delivery in good condition and her newborn examination revealed no abnormalities. Her Apgar score was 7 at 1 minute with no further assessments documented. She immediately self ventilated in low flow oxygen and no other respiratory concerns are noted.

Initial Comments from doctor:

1) Very Low Birth Weight2) ? Maternal Illness-Mum looks sick but not talking3) Severe Prematurity

Initial Management Plan:

48mls/kg/24hours 10% Dextrose Intravenously (IV)

Aminophylline, Na Bicarbonate 8.4%,

XPen, Gentamicin

1 AA will be discussed in depth as Case Study 3.2

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Keep Warm, Hb/WCC

Medical History including findings on admission (see Appendix A (p.21) for a copy of medical notes):

Baby was admitted to the special Care Nursery directly from the labour ward where it is noted that she was severely premature and was of very low birth weight at just one kilogram (kg).

Respiratory system: Baby has never had any respiratory concerns and has been self ventilating from birth and in room air for the majority of her admission with no apnoeas noted. Aminophylline IV has been being administered throughout her admission.

Circulation (A), thermoregulation (B) and fluid management (C): Few circulatory observations (other than temperature which will be discussed later) are noted in the nursing documentation and nothing at all in the medical notes. A rudimentary fluid balance chart was maintained with some omissions regarding input and no output volumes documented.

(A) On Day 3 (15/10/10) of life baby was noted to be clinically pale with Haemoglobin (Hb) of 11.8 g/dl. A cross match and blood transfusion was ordered and written instructions provided regarding its administration. On seven occasions over the proceeding fifteen days notes are entered regarding ‘chasing’ the cross match and giving the transfusion with a note on 21/10/10 stating that baby ‘looked pale +++’. Baby finally received her blood transfusion of 35mls packed red cells on 02/11/10 after a donation of blood from her father on 01/11/10. Pre-transfusion her Hb was noted to be 7.3 g/dl.

(B) Baby’s first recorded temperature in the Special Care Nursery was noted to be 38.6 degrees Celsius (C) at 06:00 on Day 2 of life. The next time her temperature is documented is at 18:00 that evening and reads 39.5 C. It can be seen from Chart 1 below that baby was only normothermic on what appears to be 9 occasions over 6 separate but non-consecutive days in her first 18 days of life. Her lowest temperature was recorded at 36.3 C and her peak temperature at 40 C. Gaps in the chart represent times when temperatures were not documented.

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(C) Baby was commenced on 48mls/kg/day of 10% Dextrose at birth which was increased to 55mls/kg/day on Day 4 of life. 36mls/kg/day of expressed breast milk (EBM) via naso-gastric tube (NGT) was also requested to be introduced. Total fluids on D4 should have been 90mls/kg/day. On D7 of life baby was still receiving 55mls/kg/day IV and NG feeds had not been commenced. It is noted that baby was active with a soft, non-distended abdomen and bowel sounds present and had regularly passed urine and had her bowels open. On D9 of life it was noted that baby was tolerating EBM via NGT at 5mls every 2 hours. Increased feeding progressed very slowly with no note of why and no note of when IV fluids are discontinued. By D17 of life baby was noted to be tolerating EBM via NGT 20mls every 2 hours (240mls/kg/day) in addition to breastfeeds. NG feeds were increased to 22mls 2 hourly (264mls/kg/day) on D17 of life with additional breastfeeds and were being tolerated at this volume at the point of my examination. Few blood glucose levels are documented but those that are were between 2.6-6 mmols/l.

Jaundice: On 20/10/10, Day 6 of life, baby was noted to be jaundiced and a Serum Bilirubin (SBR) level ordered. The first SBR levels are seen on the results sheet in Appendix B (p.30) on 19/10/10 and are 19.7 mg/dl. It is unclear from the medical and nursing notes when phototherapy was commenced but a medical note was entered on 23/10/10 for phototherapy to keep being decreased and on 26/10/10 to say that baby is out of phototherapy. SBR levels show an increase

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to 16.1 mg/dl on 29/10/10 and a subsequent downward trend to 8.2 mg/dl by 02/11/10. No further phototherapy is documented.

Weight gain: The graph below illustrates baby’s weight trend during her admission with a maximum loss of 13% of her birth weight. Gaps represent days that no weight was documented.

Neurological status: Baby is noted to be active from birth, breastfeeding early on and no neurological concerns are noted.

Family: Baby’s Mum (AA) remained in hospital with her throughout and took an active role in her care with baby’s Dad visiting when he could. AA seemed quiet and withdrawn and indicated a strong desire to return to her family and Uia village. She expressed concern that she was unable to look after the rest of her family while she was at the hospital, and for being unable to earn money in order to feed her family or afford the elder two children’s school fees. She said that the children’s father and her mother were looking after the house and garden. When questioned regarding her own health she stated that she had felt unwell throughout this pregnancy but that she felt much better since the baby had been born.

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My examination:

I examined FI of AA on 02/11/10 (D19 of life) and my findings were as follows:

Using the Dubowitz Scoring system [1] which has been validated for use in Melanesian infants [2] and with assistance from one of my fellow students, I ascertained baby’s age to be of around 34 weeks gestation ((38* 0.2642)+24.595). This would translate to a gestational age at birth of about 31 weeks which fits in with AA’s obstetric history.

Baby had recently been moved into an incubator from under a radiant warmer after receiving her blood transfusion and was self ventilating in room air with SpO2 >95% and no signs of respiratory distress. The incubator temperature was set at 35 degrees and baby was warm to touch. General findings were unremarkable, all observations being within expected limits [3] and as documented (no pre or post blood transfusion observations had been documented). Her abdomen was soft, bowel sounds were present and no liver edge or spleen were palpable.

To comment on her general condition Baby was very thin, her skin and lips were dry and her eyes were a little oedematous. When awake she was alert, looking around and handled well. She had a naso gastric tube in situ and during my visit to the unit Mum had baby out of the incubator

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and was putting her to the breast. The breast was offered for 15 minutes and then AA gave EBM via the NGT. Additionally, baby was not covered or wrapped in any way when out of the incubator.

Preterm birth and low birth weight: definitions, determinants and consequences

Infants born with a low birth weight (LBW) can be divided into two categories- those born too soon and those born too small. Preterm infants (<37 weeks gestation) have LBW primarily because they were born too soon which didn’t afford adequate time for growth and development in utero. Term infants (>37 weeks gestation) who, despite having adequate time to grow are born too small and weigh <2500g are classed as having a low birth weight [4, 5]

Further, intrauterine growth retardation/restriction (IUGR) is defined as babies with a birth weight under the 10th percentile for gestational age according to standards set by the World Health Organization [6], essentially demonstrating malnutrition at birth [5]. De Curtis et al. [7] stress the importance of considering the rate of foetal growth as compared to the norm for the relevant population and for the growth potential of a specific infant.

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WHO [8] contend that as the term LBW in itself doesn’t distinguish between a shortened gestation and sub-optimal foetal growth, it is an imperfect indicator of foetal growth and the terms ‘preterm’ and ‘IUGR’ should be employed to provide distinction. Based on this recommendation and given the parameters for being preterm and having IUGR it would be appropriate to classify our case study as both. FI of AA was born at approximately 31 weeks gestation and at 1kg weighed well under the 10th percentile of weight for gestational age.

The term ‘small for gestational age’ (SGA) is also employed in the literature and has been used as a definition of IUGR. It is however, contended to be of little value. Henrikson [9] states that a significant proportion of SGA infants are not growth retarded, nor at increased risk for poor health. The picture for both prematurity and IUGR is less positive.

Globally 8.8 million children a year die before their 5th birthday, more than 40% in their first month of life (around 450 an hour) and 99% of these are in developing countries. Of these neonatal deaths 28% are due to preterm birth; a complication which makes it one of the three most important single causes of death in under 5’s in the world [10-12].

It is estimated that 18 million babies are born with low birth weight each year comprising approximately 12% of all births in developing countries [4] and is an important indirect cause of neonatal death [10]. The high prevalence of LBW infants born in developing countries is thought to reflect proportional growth retardation rather than preterm birth [2, 13]. However, the incidence of premature delivery in IUGR infants is high and this leads to the characteristic postnatal risks of prematurity in addition to those of IUGR [14].

The regulation of foetal growth is complex and its determinants are dictated by three main variables: maternal nutritional intake, placental function and the ability of the foetus to utilise the nutrients provided [9]. In relation IUGR is characterised by insufficient transfer of nutrients and oxygen to the foetus causing impaired growth of foetal organs and tissues. IUGR may result from limited availability of maternal micro- and macro-nutrients (maternal under nutrition) or from medical conditions (e.g. infections) that impede proper vascularisation of the placenta and restrict the transfer of essential nutrients from mother to foetus [13].

In resource poor settings women are frequently under nourished and at increased risk of malaria infection making them particularly vulnerable to delivering a LBW infant [13]. Maternal malnutrition is cited as being the main causative factor of IUGR in resource poor settings [9]. Poor to non-existent antenatal care is also an important contributing factor and further, IUGR occurs most commonly in women who are of lower socioeconomic status, who access healthcare less frequently and who are not in their prime reproductive years [15].

Intra Uterine Growth Restricted infants are disadvantaged from before birth; they have a higher perinatal, neonatal and infant mortality and are at increased risk of infant, childhood and longer

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term morbidity [2,13,16,17]. Infants born with IUGR are four to ten times more likely to die in the first year of life compared to average weight for gestational age infants [15,17]

Neonatal complications found to be associated with IUGR include an increased incidence of: hypoglycaemia, hypothermia, hypocalcaemia, polycythemia, necrotizing enterocolitis, meconium aspiration and persistent foetal circulation [15]. IUGR infants also have higher rates of seizures, sepsis and respiratory failure [4] and IUGR has been shown to impair renal function in children born very preterm [18].

It is known that babies who are born with IUGR present a marked immunological deficiency compared with that of children who become malnourished after birth. It seems that this deficiency remains as IUGR babies struggle to catch up nutritionally and are subsequently more prone to infectious diseases, mainly diarrhoea, in the first two years of life [4,17].

Being born with IUGR also translates into long term growth restriction [16]. Vaughn et al [17] found that preterm babies caught up with growth at 23-47 months whereas IUGR children always had consistently lower growth rates and remained small and underweight. A lowered immunity resulting in frequent infections exacerbates impaired growth [4].

There is strong neuropathologic evidence that points to a deleterious effect of early malnutrition on brain development. IUGR involves profound deficiencies in at least three elements that are important for normal brain development: oxygen, protein-energy and iron [15]. IUGR therefore puts children at risk of neuro-developmental sequelae that may affect learning and/or social performance [4,16]. Other childhood morbidities relate to impaired maturation and disrupted organ development [14].

The foetus is known to adapt to a nutritionally deprived environment in utero by curtailing its growth. To survive, the foetus exhibits wasting in order to protect the placenta and vital organs such as the heart; the brain and adrenal glands are subsequently protected by increased blood flow. Adaptation is also demonstrated by hormone regulation being re-set to a permanently slowed rate. Thus, changes in the normal hormonal state and sensitivity of the tissues create a relationship between IUGR and abnormal structure, function, and disease in adulthood [15]. It is important to acknowledge the significance of Barker’s Hypothesis [9] suggesting that IUGR is a significant risk factor for the subsequent development of chronic hypertension, ischaemic heart disease, diabetes and obstructive lung disease in adult life.

It is estimated that 25% of infants born in Papua New Guinea are LBW. Given our knowledge of LBW statistics in resource poor countries, it can be inferred that this number largely demonstrates a higher than globally average incidence of IUGR. This would be expected to result in a considerable amount of potentially avoidable mortality and morbidity which will subsequently affect the health of future generations [2].

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Extrauterine Growth Restriction: definitions, determinants and consequences.

The possibility exists that long term neurodevelopmental deficits in IUGR infants are due in part to postnatal environmental factors rather than solely to the biological effect of foetal growth retardation on the developing foetal brain [16].

Extrauterine growth restriction (EUGR) or post natal growth failure (PNGF) refers to the phenomenon of neonates developing a severe nutritional deficit during their first weeks of life [19]. Premature, IUGR and LBW infants are at an increased risk of such a deficit [7, 19-21] but research demonstrates that EUGR presents a hazard to infants with appropriate weight for gestational age (AGA) also [21]. It is important to note that peak foetal growth occurs in the third trimester of gestation: a period when preterm infants are no longer in utero [7].

Marks et al [22] compared premature infants with IUGR infants to determine risks for EUGR. Their study demonstrates that at 31-32 weeks gestational age (GA) only 1.7% of infants experienced EUGR. Of infants weighing 1000-1249g at birth 11.4% experienced EUGR. Our baby falls into this category and so it appears that it may be her IUGR and not her prematurity that first puts her more at risk for post natal growth failure.

Metabolic and nutritional requirements of the newborn are equal to or greater than those of the foetus as adaptation to extrauterine life is an energy consumptive process [23]. Increased losses due to respiration, metabolism, thermoregulation and increased activity contribute to this. During this period of time it is asserted that many premature and IUGR infants may lose up to 15-20% of their birth weight with a prolonged period before it is regained and growth (i.e. attaining a weight beyond the birth weight) begins due to a delay in the introduction of enteral feeds [19-21,24]. Further exacerbated by their antenatal malnutrition, this period of weight loss means that these infants incur a nutritional deficit of proportions significant enough to ensure that catch up growth is nigh on impossible [23].

The American Academy of Pediatrics has suggested that optimal nutritional support of the preterm neonate should be demonstrated by postnatal growth similar to that of a normally developing foetus of the same postconceptional age [19].The objective of a nutritional regime for preterm infants should be to support life and ensure a growth rate sufficient to fulfil the individual’s genetic potential. There appear to be many controversies on how to achieve this goal [7] and optimum nutrition in the Neonatal Intensive/Special Care environment proves a challenge throughout the world [21].

The brain needs energy for cell division and growth (e.g. neuronal growth), transport via the radial glial cells, and myelination [18]. Early protein-energy deficits have far reaching effects including short stature and poor neurodevelopmental outcomes [18,23] sensory handicaps and poor school performance [19]. More acutely, severe EUGR is independently associated with

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major neonatal morbidities including respiratory distress syndrome and mechanical ventilation, patent ductus arteriosus, bronchopulmonary dysplasia and necrotizing enterocolitis [22].

Neonates who are malnourished in the postnatal period often experience immune deficiencies that reflect poor protein stores, exacerbating an already immature immune system that is further challenged due to their prematurity/IUGR. In addition to the brain and immune system, nutrients are also essential for preparing the gastrointestinal system for optimal function [19] and EUGR places infants at risk of renal impairment during childhood. EUGR coupled with prematurity represents a risk factor for long term renal impairment [18].

A number of clinical management practices have been demonstrated to contribute to neonatal malnutrition and its consequent inadequate growth and development: Fluid volume restriction [22,23] and over-conservative enteral nutrition (introduction/frequency/volumes/advancement) are among these [7,19,21]. Environmental factors are also shown to contribute to EUGR [7,18]; non nutritional facets of care such as illness and associated local management practices are suggested to account for around 50% of growth restriction [25].

Clark et al. [19] advocate that education regarding best health care practice will positively impact on better nutrition and growth and development outcomes but stress the importance of monitoring and evaluation of training and patient outcomes.

Management of Care

Regardless of what other problems they may have, all small babies require special considerations for feeding, fluid management, and maintenance of normal body temperature [26]. These principles will be discussed below taking female infant (FI) of AA’s birth weight as a guide for calculations.

WHO [26] maintain that good feeding ability can usually be attained in a neonate by 34-35 weeks post-menstrual age. Until this time a substantial effort must be made to ensure adequate nutrition involving and supporting the mother as much as possible. It is recommended that intravenous (IV) fluids of 10% Dextrose should be administered to all babies weighing <1.25kg for the first 2 days of life at 4mls/hr = 96mls/kg/24 hours. It is then recommended that expressed breast milk (EBM) be introduced on D3 via a nasogastric tube (NGT) at 3mls/2nd hourly = 108mls/kg/24 hours total fluids. IV fluids and EBM are then titrated until D7 when IV fluids are discontinued and EBM via the NGT would be at 180mls/kg/24 hours if no problems with intolerance or malabsorption were encountered.

It is noted that FI of AA was receiving 55mls/kg of IV fluids on D7 of life and enteral feeds had not been commenced (Appendix A p.21) Baby was therefore only receiving 30% of the necessary fluid requirement and little to none of her nutritional needs were being met by the end

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of her first week of life. As mentioned previously there is no note of when IV fluids were discontinued but on D10 of life baby is still only receiving 120mls/kg/24 hours of EBM via the NGT with D13 of life being the time that feeds of EBM reach the volume recommended by WHO [3,26] for D7 of life.

Although it is usual for babies to lose weight in the first 7-10 post birth even in very neonates birth weight is usually re-gained by D14 of life unless the baby has been ill [26]. Chart 2 demonstrates that FI of AA was still 10g below her birth weight on D19 of life.

If faced with inadequate growth in a neonate, in addition to increasing feed volumes WHO [3,26] recommend encouraging the mother to express her breast milk into two cups and giving the more fat rich hind milk to the infant first. A visual observation of feeding practice in SCBU at MGH demonstrated baby’s Mum first expressing the required volume of milk into a cup, then offering baby the breast and finally topping up with fore milk via the NGT after 15 minutes. Mum was unsupervised and none of the nursing staff were checking the baby’s stomach contents after breast feeds to determine how much of the hind milk was taken from the breast. Given the baby’s weight deficit it may be expected that these actions would be performed as a minimum to help try to determine why baby wasn’t gaining weight adequately. WHO recommend checking gastric aspirates for both volume/absorption and malabsorption [3].

Chart 2 also demonstrates that baby rarely achieved the 15-20g/kg day weight gain that WHO [3,26] recommend. It does in fact illustrate some rather alarming weight losses. In addition to being born with IUGR, a suboptimal nutritional regime and feeding practices seem to have contributed to a case of extrauterine growth restriction. This may well have been further compounded by the labile swings in temperature demonstrated in chart 1.

Hyperthermia can be a sign of sepsis or other illness. However, an elevated body temperature can also be indicative of exposure to a too-warm environment (e.g. high ambient temperature, overheating an incubator/radiant warmer) as neonates do not possess the thermoregulation mechanisms that older children and adults have [26]. Caution is advised in the use of incubators and radiant warmers and close monitoring, good documentation and personnel trained in their use are called for [3].

FI of AA did not ‘act’ like a baby with sepsis or who was sick (I spent a number of hours in SCBU over a period of days). She never had any respiratory concerns, became shocked or suffered from feed intolerance-all signs that one may expect to see should an infant become septic. Despite consistently having very high temperatures baby’s temperature was only checked twice daily, even when it was at its highest. WHO advocate that babies weighing <1.5kg should have their temperature taken and documented at least every six hours even if they are not unwell [3].Medical instructions to ‘reduce the infant warmer’ can be found frequently in the medical

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notes but with no further documentation regarding whether this had been done or the outcome. Baby had been placed on IV antibiotics from birth and temperatures persisted despite these. They also continued after the antibiotics were discontinued but never became worse. It may be assumed from the information present that the swinging temperatures documented are likely a result of environmental factors, poor care and baby’s lack of thermoregulatory ability rather than sepsis or other illness.

Briefly, because I feel it is of relevance to discuss it here, baby was diagnosed with jaundice on D6 of life. Over 80% of preterm infants experience some degree of jaundice [3]. If phototherapy is required WHO recommend that if an infant’s weighs <2kg phototherapy should be administered with the baby in an incubator rather than in an open cot. It is also advocated that if the baby is receiving IV fluid or EBM (which she was) then the fluid/milk should be increased by 10% of the daily total for the duration of the phototherapy. This was not done. Additionally, after D3 of life neonates require IV fluid that contains sodium in addition to glucose [3,26]. It may be that the standard unit practice was to routinely change IV fluids to Glucose + Sodium after D3 of life but this was not evident in any nursing or medical documentation.

It is important to comment that due to persistent hyperthermia and the phototherapy that was administered, baby’s metabolic rate would have been higher therefore further increasing her fluid requirements. In addition to a 10% increase in total fluid to prevent dehydration during phototherapy WHO [3,26] advocates additional fluid replacement should dehydration occur using daily weight loss as a guide. FI of AA’s dramatic weight fluctuations may demonstrate dehydration in light of increased metabolic demands in addition to poor nutrition.

In addition to fluid management, nutrition and thermoregulation issues, FI of AA experienced anaemia from birth. In areas of developing countries where maternal iron deficiency anaemia and malaria are common the prevalence of foetal anaemia is high. It is defined as a Hb of <12.5g/dl and with a Hb of 11.8g/dl our case study can be assessed as anaemic. Where the maternal prevalence of anaemia is high up to 60% of cases of foetal anaemia can be directly attributed to maternal anaemia. Foetal iron stores are already reduced in low birth weight and preterm infants. Foetal anaemia is also associated with a higher rate of mortality in LBW babies [27].

Congenital malaria (CM) is not uncommon in malaria endemic areas. The most common presenting features of congenital malaria are hepatomegaly followed by fever, splenomegaly, anaemia and jaundice. It is recommended that CM should be considered in all ill neonates where the mother has relevant risk factors. However it is important to note that clinical manifestations of CM are not normally evident at birth and it may take 2-8 weeks for symptoms to appear. [28] Although, CM has been detected at birth in preterm infants [29].

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Given AA’s history of malaria infection in her own notes, the fact that she had been sick throughout her pregnancy, was noted to be looking ill at delivery and that baby was found to be anaemic soon after birth it may have been prudent to perform malaria films on both mother and baby at the earliest possible opportunity. Pengsaa [28] highlights that initial slides may not detect parasitaemia and that blood for further slides should be taken after twelve hours. Malaria should not be ruled out until three clear smears in a 48 hour period have been obtained. Delays in diagnosis and subsequent initiation of treatment can cause significant morbidity.

Diagnosis/differential diagnosis

FI of AA was born prematurely with intrauterine growth restriction. It is likely that this was due to a set of complex variables: being the 7th child of a socioeconomically disadvantaged family living in a malaria endemic area, compounded by a complicated antenatal period leading to late presentation at ante natal clinic which further led to her mother receiving a lack of quality antenatal care.

Probable postnatal diagnosis: Poor management of care in an ‘at risk’ neonate

Differential diagnosis: Congenital malaria

Baby’s labile temperature was likely caused by immature thermoregulatory mechanisms and poor thermal management in the special care nursery. This indicates a lack of knowledge regarding the use of equipment and correct care of the at risk newborn. However, given the differential diagnosis of congenital malaria, malaria slides would have been a prudent investigation to rule this out.

The anaemia was likely attributable to maternal malnutrition but a differential diagnosis could be blood loss at birth perhaps via the umbilical cord or haemolysis, again due to congenital malaria. A number of facets of FI of AA’s management of care demonstrate a poor standard of both nursing and medical attention in this special care nursery; fluid management and nutrition, management of baby’s anaemia, documentation and communication were all lacking. The use of simple care protocols may assist in increasing the standard of care given.

Improved Management of Care

Retrospective data from Port Moresby General Hospital’s (POMGH) special care nursery (SCBU) demonstrates that, as in most other areas of the developing world, many of the LBW infants admitted were growth retarded rather than premature, although a proportion were both [30].

The duration of admission of LBW babies to SCBU was studied; the advent of Kangaroo Mother Care (KMC) and Susu Mamas (a breastfeeding support NGO) being introduced to the unit

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reflected a decrease in the duration of admission for these LBW babies. This significant decrease in length of stay was directly associated with improved weight gain in a shorter period of time which was further attributed to KMC and improved nutritional practices with the support of Susu Mamas. No Parenteral nutrition is available at POMGH.

Kangaroo Mother Care

Caring for low birth weight infants imposes a heavy burden on poor countries and Kangaroo Mother Care (KMC) has advantages for infants, mothers and health care services [31].

Kangaroo Mother Care is effectively continuous skin-to-skin contact between a mother and her infant as soon and as continuously as possible. Early and exclusive breastfeeding is advocated with expressed breast milk (EBM) given via alternative means (i.e. cup, spoon, nasogastric tube) if breastfeeding is not possible.

The literature suggests that in babies with a birth weight of 2000g or less and who are unable to regulate their own temperature KMC is at least as safe and effective as traditional incubator care and offers the ideal conditions for LBW infants to develop in. Although there is some disagreement regarding specific benefits of KMC in the literature in relation to morbidity and mortality, it has not been outperformed by standard care in any evaluation and as such is deemed to be an evidence based and sound alternative method of care for premature and LBW infants [31, 32] particularly in resource poor settings where other options are limited [33,34]. It is widely held [31,35-39] that some of the benefits that KMC offers are:

Quicker stabilization than conventional care Reduced levels of infant stress Thermoregulation that is at least as good as that provided by an incubator (if the

incubator is used correctly) A reduction in apnoeas and periodic respiration Less desaturations Higher oxygenation levels Improved neurobehaviour No additional risk of infection Both nutritive and non-nutritive suckling at the breast is introduced to preterm infants at

an earlier stage Increased production of breast milk Improvement in infant weight gain Improves parent/infant bonding Reduces morbidity in impoverished settings (e.g. due to out of date equipment or poor

practice) Earlier discharge Enhances the transition from hospital to home due to a minimal change in physical and

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Contributes to the cost efficiency of health care services

Even in non-continuous KMC, promising results have been seen in infant growth, parental attachment and a decrease in post natal depression in the infant’s mothers [40]. It is also appropriate that the role of KMC provider be shared with the baby’s father and other close family members without disrupting breastfeeding routines [31,35,38].

The review of KMC services by McMaster et al. [30] at POMGH demonstrates that the introduction of KMC to Papua New Guinea is both feasible and effective. Cattaneo et al [34] advocate that many of the annual global neonatal deaths occurring in developing countries could be prevented by appropriate, low cost and good quality care of premature and low birth weight infants. KMC is cited as an appropriate and affordable, yet high quality alternative to conventional care that is easily implemented even in small and poorly resourced hospitals. It is also strongly advocated by WHO as a safe alternative to incubator care of the low birth weight infant [3].

Summary

The aim of the UN Millennium Development Goal 4 is to reduce the mortality rate of children under five years of age by two thirds by the year 2015 [11]. Much of the world is not on target to achieve this goal; Papua New Guinea counts amongst them with an under 5 mortality rate of 69/1000 and insufficient progress to meet the goal [11,41].

Intrauterine growth restriction is of public health importance because of the strong relationship between birth weight and infant, child and later life mortality and morbidity. Targeting antenatal care is one way of trying to address this issue and will be discussed in Case Study Three. Post-birth, improving methods and standards of care in the special care environment should be seen as another.

Malnutrition in the neonatal intensive/special care environment remains common in the developed world. In the developing world it seems inevitable; nutritional solutions to EUGR suggested in the literature have little relevance to the developing world. Parenteral nutrition, breast milk fortification and speciality formulas are largely unavailable, impractical and not practicable in health care settings and not least the community post discharge. Optimising the standard of care given to infants in the developing world NICU, specifically Madang General Hospital in this particular instance and incorporating Kangaroo Mother Care into clinical practice may offer some semblance of a practicable solution to optimising the care of the premature/IUGR neonate. Adverse outcomes may be minimised and assistance given to the promotion of the improved health of future generations.

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References

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2. Primhak RA, MacGregor DF. Ethnic and environmental factors affecting fetal growth in Papua New Guinea. Annals of Human Biology 1991; 18 (3): 235-243.

3. World Health Organization. Pocket book of hospital care for children. Guidelines for the management of common illnesses with limited resources. Geneva: WHO; 2005 [cited 2011 January 10]; Online.

4. Aghamolaei T, Eftekhar H, Zare S. Risk factors associated with intrauterine growth retardation (IUGR) in Bandar Abbas. J. Med. Sci 2007; 7 (4): 665-669.

5. Muthayya S, Kurpad AV, CP Duggan CP et al. Low maternal vitamin B12 status is associated with intrauterine growth retardation in urban South Indians. European Journal of Clinical Nutrition 2006; 60: 791–801.

6. World Health Organization. Kangaroo mother care: a practical guide. Geneva: WHO; 2003 [cited 2011 Jan 10]; Online..

7. De Curtis M and Rigo J. Extrauterine growth restriction in very-low-birthweight infants. Acta Paediatrica 2004; 93: 1563-1568.

8. World Health Organization. Promoting optimal fetal development. Report of a technical consultation. Geneva: WHO; 2006 [cited 2011 Jan 10]; Online.

9. Henriksen T. Foetal nutrition, foetal growth restriction and health later in life. Acta Paediatr 1999; Suppl 429: 4-8.

10. Lawn JE, Cousens S, Zupan J. Neonatal Survival. 4 million neonatal deaths: When? Where? Why? Lancet 2005; 365: 891-900.

11. World Health Organization. Countdown to 2015 decade report (2000–2010): taking stock of maternal, newborn and child survival. Geneva: WHO; 2010 [cited 2011 Jan 10]; Online.

12. Black RE, Cousens S, Johnson HL et al. Global, regional, and national causes of child mortality in 2008: a systematic analysis. The Lancet 5 June 2010; 375: 1969-87.

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13. Landis SH, Lokomba V, Ananth CV et al. Impact of maternal malaria and under-nutrition on intrauterine growth restriction: a prospective study in Democratic Republic of Congo. Epidemiol. Infect 2009; 137: 294–304.

14. Brodsky D and Christou H. Current Concepts in Intrauterine Growth Restriction. Intensive Care Med 2004; 19: 307-319.

15. Mahajan SD, Singh S, Shah P et al. Effect of maternal malnutrition and anaemia on the endocrine regulation of fetal growth. Endocrine Research 2004; 30 (2): 189-203.

16. Georgeiff MK. Intrauterine growth retardation and subsequent somatic growth and neurodevelopment. Journal of Pediatrics 1998; 133 (1).

17. Vaughan P, Barros FC, Huttly S et al. Comparison of the causes and consequences of prematurity and intrauterine growth retardation: A longitudinal study in southern Brazil. Pediatrics 1992; 90: 238-244.

18. Bachetta J, Harambat J, Duborg L et al. Both extrauterine and intrauterine growth restriction impair renal function in children born very preterm. Kidney International 2009; 76: 445-452.

19. Clark RH, Wagner CL, Merritt RJ et al. Nutrition in the neonatal intensive care unit: how do we reduce the incidence of extrauterine growth restriction? Journal of Perinatology 2003; 23: 337–344.

20. Ernst KD, Radmacher PG, Rafail ST et al. Postnatal malnutrition of extremely low birth-weight infants with catch-up growth post discharge. Journal of Perinatology 2003; 23: 477–482.

21. Radmacher PG, Looney SW, Rafail S et al. Prediction of extrauterine growth retardation (EUGR) in VVLBW infants. Journal of Perinatology 2003; 23: 392–395.

22. Marks KA, Reichman B, Lusky A et al. Fetal growth and postnatal growth failure in very-low-birthweight infants. Acta Paediatrica 2006; 95: 236-242.

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25. Embleton NE, Pang N, Cooke RJ. Postnatal malnutrition and growth retardation: an inevitable consequence of current recommendations in preterm infants? Pediatrics 2001; 107 (2): 270–3.

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26. World Health Organization. Managing newborn problems: a guide for doctors, nurses, and midwives. Geneva: WHO; 2003 [cited 2010 Sept 13]; Online.

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28. Pengsaa K. Congenital malaria in Thailand. Annals of Tropical Paediatrics 2007; 27: 133–139.

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33. Lawn JE, Mwansa-Kambafwile J, Horta BL et al. Kangaroo Mother Care to prevent neonatal deaths due to preterm birth complications. International Journal of Epidemiology 2009; 39 (Suppl. 1): i144–i154.

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40. Ahn HY, Lee J, Shin HJ. Kangaroo Care on Premature Infant Growth and Maternal Attachment and Post-partum Depression in South Korea. Journal of Tropical Paediatrics 2010; 56 (5): 342-344.

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Appendix A

FI of AA’s notes (copied directly from medical notes)

16/10/10

Weight:

Nil else documented.

17/10/10 D2 (D3)

Weight: 1.05kg (-70g)

Temperature (T):

Pulse (P):

Respirations (R):

No apnoeas, clinically pale, Hb 11.8, abdomen soft, bowel sounds heard, PU/BO

Plan:

X-match and transfuse. Transfusion order: 35mls blood over 4 hours with diuretic stat dose

Continue IVI at same rate

NBM

Zinc ½ tablet

18/10/10 D3

Weight 1kg (-50g)

T:

P:

R:

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Pale ++, active, abdomen distended, bowel sounds present, Not had blood yet

Plan:

NBM

Increase IVI to 2.3mls/hr (55mls/kg)

Follow up x-match and transfuse

Decrease infant warmer

Start feeds 3mls EBM via NGT every 2 hours (36mls/kg)

Total fluids 90mls/kg/24hrs

19/10/10

Weight: 1kg

T:

P:

R:

Abdomen soft, PU/BO

Plan:

Chase x-match

Continue treatment

My note: Feeds not started, remains NBM

20/10/10 D5

Weight: 940g (-60g)

T:

P:

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R:

Abdomen soft, PU/BO, jaundice, Still NBM

Plan:

Continue all treatment

SBR

21/10/10 D6 My note: different doctor

Weight: 960g (+20g)

T:

P:

R:

No apnoeas, pale++, jaundiced, active, abdo soft, bowel sounds heard

Plan:

Chase cross match and transfuse

Start Feeds

22/10/10 D7

Weight: 1.010kg (+50g)

T: 39.2

P:

R:

Active, pale++, less jaundiced

Plan:

Reduce infant warmer

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NG feeds

Continue treatment

SBR

23/10/10 D8

Weight: 1.010kg (static)

T: 39.1

P:

R:

Pale, jaundiced, eyes ok, abdomen soft, bowel sounds heard, moving all limbs, SBR not done, tolerating 5mls/2nd hr EBM

Plan:

Increase feeds to 8mls 2nd hrly

Keep reducing PT

SBR

Needs blood transfusion

Stop Gentamicin

24/10/10 D9

Weight: 1.020kg (+10g)

T:

P:

R:

Less jaundiced, active, tolerating 5mls EBM 2nd hrly

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Plan:

Decrease infant warmer

Increase feeds to 8mls 2nd hrly

Intermittent PT when SBR known

Needs blood

25/10/10 D10

Weight: 1.010kg (-10g)

T:

P:

R:

Tolerating feeds well and breast feeding, D10 of Penicillin-last day of ABX

Plan:

Increase feeds to 10mls 2nd hrly

SBR and cont PT

26/10 D11

Weight: 1.020kg (+10g)

T:

P:

R:

Tolerating feeds, not jaundiced now, PU/BO, active, abdo soft, CVS ok, SBR 25/10 not available

Plan:

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Out of phototherapy, increase feeds to 12mls 2nd hrly, chase SBR, keep warm, needs blood transfusion

27/10/10 D12

Weight: 1.010kg (-10g)

T:

P:

R:

Tolerating NG feeds, breastfeeding well, PU/BO

Plan:

Await blood transfusion

28/10/10 D13

Weight: 1.020kg (+10g)

T:

P:

R:

Breastfeeding well, PU/BO, slight jaundice

Plan:

Increase NG feeds to 16mls 2nd hrly

Continue treatment

SBR

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29/10/10 D14

Weight: 870g (-150g)

T:

P:

R:

Tolerating feeds, PU/BO

Plan:

SBR

30/10/10 D15

Weight: 870g (static)

T:

P:

R:

Tolerating 18mls NG 2nd hrly, Mum not lactating well (prescribed Maxalon), active, pale, jaundiced, abdo soft, good BS.

Plan:

Increase feeds to 20mls 2nd hourly (240mls/kg/24), father to donate blood 1/11, continue PT

31/10/10 D16

Weight: 920g (+50g)

T:

P:

R:

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Tolerating feeds, mum lactating well, slight jaundice, abdo soft

Plan:

Increase feeds to 22mls 2nd hrly

SBR

01/11/10 D17

Weight: 950g (+30g)

T:

P:

R:

Tolerating feeds, less jaundiced, active, pale

Plan:

Continue with PT

SBR

Same feeds

2/11/10 D 18

Weight: 990g (+40g)

T:

P:

R:

Tolerating feeds, father has donated blood

Plan:

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SBR and continue PT

Continue feeds

Transfuse today

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Appendix B

FI of AA Results Chart

Date SBR Hb Wcc2/11 d19 8.2 7.3 12.81/11 d18 9.729/10 d15 16.128/10 d14 15.622/10 d8 15.920/10 d6 19.716/10 d2 11.8 13.8

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