2013 Fluid Homeostasis in the Neonate | Preterm Birth | Intravenous Therapy

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  REVIEW ARTICLE Fluid homeostasis in the neonate Frances O’Brien 1 & Isabeau A. Walker 2,3 1 Department of Paediatrics, John Radcliffe Hospital, Oxford University Hospitals NHS Trust, Headington, Oxford, UK2 UCL Institute of Child Health, London, UK3 Department of Anaesthesia, Great Ormond Street Hospital NHS Foundation Trust, London, UK Keywords neonate; fluids; salt solutions; colloids;blood transfusion; NICU Correspondence Isabeau A. Walker, Department ofAnaesthesia, Great Ormond Street HospitalNHS Foundation Trust, Great OrmondStreet, London WC1N 3JH, UKEmail: isabeau.walker@gosh.nhs.ukSection Editor: Andy WolfAccepted 12 November 2013doi:10.1111/pan.12326 Summary The physiology of the neonate is ideally suited to the transition to extrauter-ine life followed by a period of rapid growth and development. Intravenousfluids and electrolytes should be prescribed with care in the neonate. Sodiumand water requirements in the first few days of life are low and should beincreased after the postnatal diuresis. Expansion of the extracellular fluid vol-ume prior to the postnatal diuresis is associated with poor outcomes, particu-larly in preterm infants. Newborn infants are prone to hypoglycemia andrequire a source of intravenous glucose if enteral feeds are withheld. Anemiais common, and untreated is associated with poor outcomes. Liberal versusrestrictive transfusion practices are controversial, but liberal transfusionpractices (accompanied by measures to minimize donor exposure) may beassociated with improved long-term outcomes. Intravenous crystalloids areas effective as albumin to treat hypotension, and semi-synthetic colloids can-not be recommended at this time. Inotropes should be used to treat hypoten-sion unresponsive to intravenous fluid, ideally guided by assessment of perfusion rather than blood pressure alone. Noninvasive methods of assess-ing cardiac output have been validated in neonates. More studies are requiredto guide fluid management in neonates, particularly in those with sepsis orundergoing surgery. A balanced salt solution such as Hartmann’s or Plasma-lyte should be used to replace losses during surgery (and blood or coagulationfactors as indicated). Excessive fluid administration during surgery should beavoided. Introduction In the neonate, fluid homeostasis is determined by thephysiological demands of transition to extrauterine lifeand the period of rapid growth and development in thefirst few weeks and months after birth. Prematurityimposes additional challenges due to incomplete organdevelopment. For the anesthetist, administration of intravenous fluids to maintain cardiovascular stability isone of the most basic interventions in pediatric anesthe-sia, yet practical evidence-based guidelines concerningintravenous fluid management are surprisingly difficultto find. Much of the literature regarding fluid homeosta-sis in neonates relates to neonatal intensive care (in par-ticular management of preterm neonates), where it hasbeen shown that excessive intravenous fluid is harmful,particularly in the first few days of life. Intravenous fluidmanagement can be particularly challenging in neonateswith sepsis or in those undergoing a major surgical inter-vention. In adult perioperative practice, it is now estab-lished that fluid management strategies have animportant effect on long-term outcomes, and it is likelythat this is also the case in children, particularly inneonates (1,2).This article revises some of the basic physiologicalprinciples underlying fluid management in neonates, theparticular considerations of preterm infants, and thechanges that occur around the time of birth. We describea practical approach to intravenous fluid management inthe neonatal intensive care unit and during the perioper-ative period, including the principles underlying the useof crystalloids, colloids, and blood transfusion. ©   2013 John Wiley & Sons LtdPediatric Anesthesia  24  (2014) 49–59 49 Pediatric Anesthesia ISSN 1155-5645  Fluid compartments and the capillary endothelialglycocalyx model Fluid homeostasis in adults has been reviewed recently(3,4). Water comprises 60% of lean body mass; two-thirds of body water is intracellular and about one-thirdis in the extracellular fluid (ECF) compartment. Sodiumis the principle extracellular cation and chloride theprinciple anion; potassium and phosphate are the princi-ple intracellular cations and anions respectively, andthere is a high intracellular protein content. Transmem-brane ion channels and electrochemical gradients main-tain the distribution of ions, and movement of wateracross semipermeable cell membranes maintains osmoticequilibrium. Water and sodium homeostasis is main-tained by the balance between intake and losses(measured and insensible), thirst, and the activity of the renin-angiotensin-aldosterone system, natureticpeptides, and antidiuretic hormone.The ECF is divided into intravascular fluid (contain-ing plasma and cellular constituents of blood) and theinterstitial fluid compartments. Movement of fluid(including proteins) between the intravascular and theinterstitial fluid compartment is crucially dependent onthe capillary endothelium and the overlying capillaryendothelial glycocalyx, which together form theendothelial glycocalyx layer (EGL). The endothelialglycocalyx consists of glycoproteins and proteoglycanscontaining glycosaminoglycans attached to the endolu-minal surface of the capillary endothelium. Albumin iscontained within the glycocalyx layer, and the endothe-lial glycocalyx layer requires a normal level of plasmaalbumin to function.The vascular endothelium/glycocalyx barrier is freelypermeable to water, semipermeable to albumin, butimpermeable to large protein molecules ( > 70 kDa) inplasma. Sodium and chloride ions pass freely into theinterstitial fluid via ion channels in the capillary endo-thelium. The colloid osmotic pressure and hydrostaticpressure in the interstitial fluid are low, and under nor-mal circumstances, outward hydrostatic pressure fromthe lumen of the capillary and the (smaller) inward pullof the colloid osmotic pressure from the capillary resultsin a continuous net outward leak of protein and fluidthroughout the length of the capillary into the intersti-tial fluid; this is cleared from the interstitial space aslymph so as to avoid the accumulation of interstitialedema.The EGL has an important role in inflammation,hemostasis, and regulation of vasomotor tone. Theendothelial glycocalyx (EGC) is fragile and is damagedby rapid infusion of intravenous fluids, surgery,ischemia, hypoxia, inflammatory cytokines, and acutehyperglycemia; the net result is an increase in vascularpermeability and increased loss of plasma protein,including albumin into the interstitial space, whichresults in interstitial edema. This transcapillary leak of albumin may be greatly increased in shock. Various sub-stances have been shown to protect the EGC (sevoflura-ne, hydrocortisone, and antithrombin III) and mayconfer therapeutic benefit.When capillary hydrostatic pressure is low, the tran-scapillary leak ceases. When intravenous fluid is given(crystalloid or colloid), it is retained in the intravascularvolume initially until hydrostatic pressure increases andfiltration into the interstitial space is resumed; thus,crystalloids should theoretically be as effective as col-loids in hypovolemic fluid resuscitation, rather than thetraditional 3 : 1 volume ratio, and this is born out inclinical studies (see below). However, if colloid is givenin the euvolemic state, it is retained in the plasma vol-ume causing hemodilution and a fall in hematocrit,increases transcapillary filtration, and potentially causesdisplacement of albumin into the interstitium. A crystal-loid solution also increases hydrostatic pressure andtranscapillary filtration, but reduces colloid osmoticpressure so that fluid filtration is increased to a greaterextent than with a colloid infusion, and there is lessmarked hemodilution. Fluid compartments in the neonate In utero , the fetus exists in a fluid filled environment  —  the major determinant of fluid balance is placentalblood flow and later in development, absorption of amniotic fluid through the gastrointestinal tract. Earlyin fetal life, 90% of the body weight is water, and theECF fluid volume is expanded, representing 60% of body weight. As the fetus develops, naturesis and diure-sis result in contraction of the interstitial fluid volumeso that by term, water comprises 75% of body weightand the ECF fluid volume comprises 40% of bodyweight (5,6). Contraction of the interstitial fluid volumecontinues through infancy and early childhood suchthat the adult distribution of total body water isobtained by 10 years of age (6). Preterm birth has amajor effect on body water composition; water repre-sents 90% of the body weight of a baby born at23 weeks gestational age (GA), and 80  –  85% of the bodyweight of a baby born at 25  –  30 weeks (7) (see Table 1).The normal blood volume in the neonate is approxi-mately 80 ml  kg  1 (depending on the time the cord isclamped), approximately 100 ml  kg  1 in preterminfants. ©   2013 John Wiley & Sons LtdPediatric Anesthesia  24  (2014) 49–59 50 Fluid homeostasis in the neonate  F. O’Brien and I.A. Walker  Neonatal physiology and cardiorespiratoryadaptation after birth Cardiorespiratory adaptation Birth represents a time of profound physiologicalchange as placental blood flow ceases and the baby tran-sitions to independent life. The fetal lungs are filled withfluid, and production of fetal lung water ceases duringlabor; liquid is squeezed out of the lungs during the sec-ond stage of delivery, but most of the fetal lung water isabsorbed into the pulmonary capillaries and lymphaticsas the first breaths are taken. Oxygen tension rises andpulmonary vascular resistance falls. This period of car-diorespiratory adaptation also involves closure of thefetal shunts (foramen ovale, ductus venosus, and ductusarteriosus). The ductus arteriosus constricts as oxygentension rises and, in most term babies and ‘well’ pretermbabies, is closed functionally by 2 days of life, with ana-tomical closure by 2  –  3 weeks. The ductus arteriosusmay remain patent if oxygen tensions are low, or in thepresence of sepsis, acidosis, or high circulating prosta-glandin levels. Patent ductus arteriosus (PDA) is com-mon in preterm infants for these reasons and is seen in50% of preterm neonates with birth weight  < 800 g.PDA results in left to right shunt, increased pulmonaryblood flow and increased risk of chronic lung disease,necrotizing enterocolitis (NEC), and poorer long-termoutcomes (8). The incidence of PDA is affected by intra-venous fluid management during this vulnerable period,as will be described below. The postnatal diuresis Fluid requirements are low in the first few days of life inthe term neonate. Breast-feeding is becoming establishedand urine output is low due to the high levels of circulat-ing vasopressin around the time of birth. In the first fewdays after birth pulmonary vascular resistance continuesto fall and pulmonary venous return increases, thiscauses release of atrial naturetic peptide, which in turnresults in a brisk diuresis (9). The postnatal diuresis isassociated with contraction of the ECF due to the lossof isotonic fluid from the interstitial fluid compartmentand a reduction in body weight of 5  –  10% in healthyterm babies. Weight is usually at a nadir around day 5,but most babies regain their birth weight between 7 and10 days. Weight loss of 10  –  15% may occur in the firstweek of life during postnatal adaptation in preterminfants ( < 27 weeks GA), and they may take longer toregain their birth weight.Expansion of the ECF by excessive administration of sodium and water, particularly before the postnataldiuresis has occurred, has an adverse effect on out-comes, particularly in extremely low birth weight infants(10  –  14). A Cochrane review of randomized controlledstudies comparing liberal to restricted water (andsodium) intake in preterm neonates demonstrated a sig-nificant increase in postnatal weight gain, and increasedrisk of PDA and NEC, with a trend to increased risk of bronchopulmonary dysplasia, intracranial hemorrhage,and death (11). A retrospective chart review of 204 neo-nates  < 32 weeks GA from a single institution suggestedrestricted water intake in the first 3 days of life (constantcalorie intake) was protective for the development of PDA, with the difference remaining after controlling forgestational age and severity of illness (14). A random-ized controlled trial in neonates  < 30 weeks GA showedthat early sodium supplementation (4 mmol  kg  1  day  1 ) was associated with delayed postnatal diuresis,delayed reduction in ECF, and increased oxygenrequirement at 1 month (12,13). Renal function in the neonate After the postnatal diuresis, the neonate grows rapidly.Renal function is ideally adapted to cope with a liquid(milk) diet with relatively low sodium content. Sodiumis required for growth and is retained avidly in the distaltubules under the influence of the renin-angiotensin-aldosterone system (RAAS). Although the kidney has afull complement of nephrons from around 35 weeks ges-tation, the renal tubules are short and there is limitedability to concentrate the urine (6). High volumes of dilute urine are therefore produced (urinary osmolality300 mOsmol  kg  1 ) at a rate of around 2  –  3 ml  kg  1  h  1 (45  –  50 ml  kg  1  day  1 ). Neonates are also able to pro-duce more dilute urine in the face of a high water load(provided ADH levels are not elevated), but they havelimited ability to concentrate the urine, so become dehy-drated easily (11). Growth of the kidney is associatedwith increasing complexity and length of the renaltubules, and increasing ability to concentrate the urine,so that by a year of age, infants are able to vary the con-centration of urine between 50 and 1400 mOsmol  kg  1 ,as in adults (6). Table 1  Variation in total body water composition and extracellularfluid (ECF) volume at birth in relation to gestational age and bodyweightGestational age(weeks)Bodyweight (BW) (g)Total bodywater (%BW)ECF volume(%BW)23  –  27 500  –  1000 85  –  90 60  –  7028  –  32 1000  –  2000 82  –  85 50  –  6036  –  40  > 2500 71  –  76  ~  40 ©   2013 John Wiley & Sons LtdPediatric Anesthesia  24  (2014) 49–59 51 F. O’Brien and I.A. Walker  Fluid homeostasis in the neonate  Neonates are susceptible to disorders of sodium bal-ance, and both sodium and water content in intravenousfluids need to be considered carefully. Aldosterone secre-tion is slow to be reduced in the face of a sodium load,for instance from isotonic fluid boluses, intravenousflushes, and drugs, and may result in hypernatremia orsodium retention with edema formation. It is recom-mended that neonates are given sodium-free fluids untilafter the postnatal diuresis to allow for contraction of the ECF volume (12,13), but inadequate sodium intakethereafter will result in hyponatremia. This is particu-larly important in preterm neonates as the RAAS isless active, and they have a limited ability to retainsodium in the distal renal tubule. Inadequate sodiumintake is associated with severe hyponatremia and poorlong-term neurological outcomes in preterm neonates(16). Insensible water loss in neonates In adults, insensible water loss (IWL) consists mostlyof water lost via evaporation through the skin (two-thirds) or respiratory tract (one-third). In neonates,IWL from the skin varies with gestational age; themore preterm the infant, the greater the transepidermalwater loss as there is a higher body surface area toweight ratio, and the skin in the most preterm neonatesis thin and fragile and poorly keratinized. Use of aradiant warmer or phototherapy significantly increasesIWL and can have a significant affect on fluid balance.In extreme preterm infants, IWL losses may exceedrenal water losses (15). Evaporation of water from theskin is associated with cooling due to the effect of thelatent heat of evaporation. Difficulty in keeping a babywarm may be an indication of excessive IWL. IWLmay be reduced by nursing preterm infants  < 2 weeks of age in a heated humidified incubator ( > 80% humidity),but if the baby is taken out of the incubator (forinstance for surgery) or if the incubator is left open forprocedures, this protection will be lost. Insensible waterloss decreases as preterm neonates mature, and ambienthumidity may be gradually decreased with time. Theincidence of hypernatremic dehydration and tempera-ture instability in preterm infants are good indicatorsof the quality of nursing care in a neonatal intensivecare unit.Humidification reduces IWL from the lungs in venti-lated babies, and humidification is also required forbabies receiving nasal CPAP or nasal ‘high flow’therapy. Postextubation, respiratory IWL may be highif a neonate receives unhumidified oxygen via nasalcannulae. Nutritional requirements Fluid requirements cannot be considered in isolationfrom nutritional requirements, particularly the require-ments for glucose, although a detailed consideration isbeyond the remit of this article. Blood glucose fallsimmediately after birth, but rises in the first few hours inresponse to endogenous glucose production or feeding.Neonates metabolize ketones as well as glucose as animportant energy substrate in the brain, so are relativelyprotected from damage due to hypoglycemia. However,prolonged hypoglycemia below 2.6 mmol  l  1 is associ-ated with abnormal neurological outcomes. Pretermneonates are at risk of hypoglycemia if enteral feeding isdelayed (for example, to reduce the risk of NEC), andthey have limited glycogen stores. Intravenous glucoseshould be provided to babies at risk of hypoglycemia ata starting rate of 5  –  7 mg  kg  1  min  1 (10% dextrose70  –  100 ml  kg  1  day  1 ), and blood glucose should bemonitored (15). Blood transfusion Anemia is common in neonates in the NICU, partly dueto the transition from synthesis of fetal hemoglobin toadult hemoglobin A that starts at birth, limited respon-siveness to erythropoietin in the neonate, and rapidgrowth. Anemia is also related to timing of clamping of the umbilical cord at birth, iatrogenic anemia fromrepeated blood samples in the NICU, sepsis, and surgi-cal interventions (17,18).Untreated anemia is associated with apnea, poorweight gain, and poor neurodevelopmental outcomes.It has also been suggested that prior blood transfusionmay be a risk factor for NEC, particularly in extremepreterm neonates, although the precise mechanism isnot clear. Suggestions include alterations in gut perfu-sion associated with feeding in neonates with hemody-namically significant PDA, the severity of preexistinganemia, or immunological mechanisms associated withthe transfusion of red cells without leukocyte deple-tion (19,20). Interestingly, neonates are also dispropor-tionately represented in the UK Serious Hazards of Blood Transfusion reporting system, primarily relatedto misidentification (lack of wrist bands), and overtransfusion (18). As neonates are such frequent recipi-ents of blood transfusions, questions arise as to whattrigger for transfusion should be used, what should bethe target hemoglobin, and how to minimize donorexposure. Hemostasis in neonates is discussed else-where in this journal and will not be considered here(21). ©   2013 John Wiley & Sons LtdPediatric Anesthesia  24  (2014) 49–59 52 Fluid homeostasis in the neonate  F. O’Brien and I.A. Walker
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