Polycythemia of the Newborn

Polycythemia of the Newborn

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The term polycythemia means an increased cell number. However, it is mostly used to refer specifically to increased circulating red blood cell (RBC) mass. RBC mass is estimated using the hematocrit (Hct) measurement, which is defined as the percentage of RBCs in a given volume of blood. Term newborns usually have a higher Hct (51 ± 7%) compared to older children and adults. This increased Hct is a normal compensatory mechanism in these infants for the relative tissue-level hypoxia that is prevalent in the intrauterine environment, and it is exacerbated by the high affinity of fetal hemoglobin for oxygen. [1, 2]  Polycythemia in the newborn is defined as a central venous Hct over 65% or a hemoglobin value above 22 g/dL.

Most of the clinical significance of polycythemia is related to the associated increase in blood viscosity. [3]  Blood viscosity increases linearly with increased hematocrit (Hct), but it can increase exponentially when Hct is greater than 42%. In addition to RBC mass several other factors also determine blood viscosity. [4]  These include blood pH, red blood cell (RBC) deformability, plasma protein concentration, platelet and white blood cell (WBC) volume as well as endothelial factors. Most of these factors are not significantly different between infants who are otherwise well. Therefore, RBC mass (or Hct) is the primary determinant of neonatal blood viscosity, and up to 50% of infants with polycythemia have hyperviscosity, although only 24% of infants with hyperviscosity have a diagnosis of polycythemia. [5]

Because the increased viscosity of a fluid and a smaller radius of the conduit through which it flows can increase the internal resistance of the fluid according to Poiseuille’s law, polycythemia-induced hyperviscosity increases the resistance of blood to flow, especially in the microcirculation. The resultant decreased microcirculatory perfusion and increased risk for thrombosis and ischemia of end organs are the factors responsible for most of the complications associated with polycythemia. Increased blood viscosity can cause hypoperfusion directly by decreasing blood flow (as is seen in the lungs and the renal system), whereas other organs can become hypoperfused due to changes in arterial oxygen content (as noted in the brain). [6]

Increased circulating red blood cell (RBC) mass in the newborn could be secondary to actively increased RBC production by the fetus or the newborn, or due to passive transfusion of RBCs into the fetal or neonatal circulation. 

Increased fetal erythropoiesis is usually a fetal response to intrauterine stress and fetal hypoxia associated with increased fetal oxygen consumption resulting in fetal hypoxia that could be related to several primary etiologic factors. Most of these conditions are also associated with intrauterine growth restriction (IUGR). Underlying causes include the factors outlined below.

Placental insufficiency

Placental insufficiency could be secondary to the following:


Primary renovascular disease

Chronic or recurrent abruptio placenta

Maternal cyanotic congenital heart disease

Postdate pregnancy

Maternal smoking

Endocrine abnormalities

These include congenital thyrotoxicosis and maternal diabetes with poor glycemic control.

Genetics disorders

Genetic conditions that increase fetal erythropoiesis include the following:

Trisomy 13

Trisomy 18

Trisomy 21

Beckwith-Wiedemann syndrome

Polycythemia-hyperviscosity could also be secondary to increased blood volume secondary to transfusion of blood either from maternal or sibling fetal sources.

Placental-fetal transfusion

Animal studies have suggested that acute fetal hypoxia can lead to increased fetal blood volume before birth, but this is unlikely to lead to significant polycythemia. [7]  Delayed cord clamping (DCC) allows for an increased blood volume to be delivered to the infant. When cord clamping is delayed more than 3 minutes after birth, blood volume increases 30%. However, potential complications of DCC include polycythemia and hyperbilirubinemia. [8] Gravity, because of the position of the delivered infant in relation to the maternal introitus, and oxytocin release could also be causative factors that increase the voulme of blood that is transfused into the newborn infant’s circulation during DCC.

Several studies have examined the incidence of polycythemia as a potential complication when DCC is practiced. A study of 242 newborns whose cords were clamped at less than 60 seconds, between 1 minute and just under 2 minutes, or between 2 and 3 minutes following birth found that their hematocrit (Hct) values at 48 hours after birth were 53%, 58% and 59% respectively. [9] Ferritin and hemoglobin levels also increased in association with later cord clamping. In addition, the number of infants with polycythemia was significantly higher in the group that was clamped at 2-3 minutes, but none of the infants from any of these groups required treatment for symptoms related to polycythemia-hyperviscosity. [9]

A more recent study of 73 infants showed that DCC at 5 minutes after birth did not lead to an increased incidence of polycthemia when compared to early cord clamping. [10]  Another study that compared early cord clamping before 10 seconds after delivery with DCC at 3 minutes or later found no differences in the incidence of polycthemia at age 4 months in these infants. [11]  Thus, although DCC increases Hct levels, currently available evidence indicates that there is minimal risk for symptomatic polycythemia that requires management.

Twin-to-twin transfusion syndrome

Twin-to-twin transfusion syndrome (TTTS) due to a vascular communication occurs in approximately 10% of monozygotic twin pregnancies. In intrapartum asphyxia, blood volume is shifted from the placenta to the fetus.

Monochorionic diamniotic (MCDA) twin pregnancies with amniotic fluid discordance appear to increase the risk of development of twin anemia-polycythemia sequence (TAPS), a form of TTTS, by nearly two-fold. [12]

Polycythemia is a relatively common disorder, occurring in 1-5%% of neonates. [13] It is more common in infants who are small for their gestational age (SGA) and in infants who are large for their gestational age (LGA). Infants born at higher elevations also have a higher incidence. However, most infants with polycythemia are of appropriate size or weight for their gestational age (AGA). Infants of mothers with diabetes have a polycythemia incidence of 10-30%.

The central venous hematocrit (Hct) level peaks 6-12 hours after birth and then declines until the infant is aged 24 hours, at which time it equals the Hct level in cord blood. Fewer than 40% of infants with a Hct level above 64% at 2 hours still have a high value at 12 hours or later.

Jopling J, Henry E, Wiedmeier SE, Christensen RD. Reference ranges for hematocrit and blood hemoglobin concentration during the neonatal period: data from a multihospital health care system. Pediatrics. 2009 Feb. 123 (2):e333-7. [Medline].

Kates EH, Kates JS. Anemia and polycythemia in the newborn. Pediatr Rev. 2007 Jan. 28 (1):33-4. [Medline].

Jeevasankar M, Agarwal R, Chawla D, Paul VK, Deorari AK. Polycythemia in the newborn. Indian J Pediatr. 2008 Jan. 75 (1):68-72. [Medline].

Mimouni FB, Merlob P, Dollberg S, Mandel D. Neonatal polycythaemia: critical review and a consensus statement of the Israeli Neonatology Association. Acta Paediatr. 2011 Oct. 100(10):1290-6. [Medline].

Drew JH, Guaran RL, Cichello M, Hobbs JB. Neonatal whole blood hyperviscosity: the important factor influencing later neurologic function is the viscosity and not the polycythemia. Clin Hemorheol Microcirc. 1997 Jan-Feb. 17 (1):67-72. [Medline].

Rosenkrantz TS. Polycythemia and hyperviscosity in the newborn. Semin Thromb Hemost. 2003 Oct. 29(5):515-27. [Medline].

O W, Omori K, Emmanouilides GC, Phelps DL. Placenta to lamb fetus transfusion in utero during acute hypoxia. Am J Obstet Gynecol. 1975 Jun 1. 122 (3):316-22. [Medline].

Fogarty M, Osborn DA, Askie L, et al. Delayed vs early umbilical cord clamping for preterm infants: a systematic review and meta-analysis. Am J Obstet Gynecol. 2017 Oct 30. [Medline].

Rincon D, Foguet A, Rojas M, et al. [Time of cord clamping and neonatal complications, a prospective study] [Spanish]. An Pediatr (Barc). 2014 Sep. 81 (3):142-8. [Medline].

Mercer JS, Erickson-Owens DA, Collins J, Barcelos MO, Parker AB, Padbury JF. Effects of delayed cord clamping on residual placental blood volume, hemoglobin and bilirubin levels in term infants: a randomized controlled trial. J Perinatol. 2017 Mar. 37 (3):260-264. [Medline].

Andersson O, Hellstrom-Westas L, Andersson D, et al. Effect of delayed versus early umbilical cord clamping on neonatal outcomes and iron status at 4 months: a randomised controlled trial. BMJ. 2011 Nov 15. 343:d7157. [Medline]. [Full Text].

Hiersch L, Eitan M, Ashwal E, et al. Amniotic fluid discordance in monochorionic diamniotic twin pregnancies is associated with increased risk for twin anemia-polycythemia sequence. Prenat Diagn. 2016 Dec. 36 (12):1099-103. [Medline].

Vlug RD, Lopriore E, Janssen M, et al. Thrombocytopenia in neonates with polycythemia: incidence, risk factors and clinical outcome. Expert Rev Hematol. 2015 Feb. 8 (1):123-9. [Medline].

Dempsey EM, Barrington K. Short and long term outcomes following partial exchange transfusion in the polycythaemic newborn: a systematic review. Arch Dis Child Fetal Neonatal Ed. 2006 Jan. 91(1):F2-6. [Medline].

OETTINGER L Jr, MILLS WB. Simultaneous capillary and venous hemoglobin determinations in the newborn infant. J Pediatr. 1949 Sep. 35 (3):362-5. [Medline].

Verbeek L, Slaghekke F, Sueters M, et al. Hematological disorders at birth in complicated monochorionic twins. Expert Rev Hematol. 2017 Jun. 10 (6):525-32. [Medline].

Sankar MJ, Agarwal R, Deorari A, Paul VK. Management of polycythemia in neonates. Indian J Pediatr. 2010 Oct. 77(10):1117-21. [Medline].

Sundaram M, Dutta S, Narang A. Fluid supplementation versus no fluid supplementation in late preterm and term neonates with asymptomatic polycythemia: a randomized controlled trial. Indian Pediatr. 2016 Nov 15. 53 (11):983-6. [Medline].

[Guideline] AAP. American Academy of Pediatrics Committee on Fetus and Newborn: Routine evaluation of blood pressure, hematocrit, and glucose in newborns. Pediatrics. 1993 Sep. 92 (3):474-6. [Medline].

Morag I, Strauss T, Lubin D, Schushan-Eisen I, Kenet G, Kuint J. Restrictive management of neonatal polycythemia. Am J Perinatol. 2011 Oct. 28(9):677-82. [Medline].

Sainz JA, Romero C, Garcia-Mejido J, Soto F, Turmo E. Analysis of middle cerebral artery peak systolic velocity in monochorionic twin pregnancies as a method for identifying spontaneous twin anaemia-polycythaemia sequence. J Matern Fetal Neonatal Med. 2014 Jul. 27 (11):1174-6. [Medline].

Veujoz M, Sananes N, Severac F, et al. Evaluation of prenatal and postnatal diagnostic criteria for twin anemia-polycythemia sequence. Prenat Diagn. 2015 Mar. 35 (3):281-8. [Medline].

Awonusonu FO, Pauly TH, Hutchison AA. Maternal smoking and partial exchange transfusion for neonatal polycythemia. Am J Perinatol. 2002 Oct. 19(7):349-54. [Medline].

Drew JH, Guaran RL, Grauer S, Hobbs JB. Cord whole blood hyperviscosity: measurement, definition, incidence and clinical features. J Paediatr Child Health. 1991 Dec. 27(6):363-5. [Medline].

Pappas A, Delaney-Black V. Differential diagnosis and management of polycythemia. Pediatr Clin North Am. 2004 Aug. 51(4):1063-86, x-xi. [Medline].

Schimmel MS, Bromiker R, Soll RF. Neonatal polycythemia: is partial exchange transfusion justified?. Clin Perinatol. 2004 Sep. 31(3):545-53, ix-x. [Medline].

Shohat M, Reisner SH, Mimouni F, Merlob P. Neonatal polycythemia: II Definition related to time of sampling. Pediatrics. 1984 Jan. 73(1):11-3. [Medline].

Werner EJ. Neonatal polycythemia and hyperviscosity. Clin Perinatol. 1995 Sep. 22(3):693-710. [Medline].

Wirth FH, Goldberg KE, Lubchenco LO. Neonatal hyperviscosity: I. Incidence. Pediatrics. 1979 Jun. 63(6):833-6. [Medline].

Wong W, Fok TF, Lee CH, et al. Randomised controlled trial: comparison of colloid or crystalloid for partial exchange transfusion for treatment of neonatal polycythaemia. Arch Dis Child Fetal Neonatal Ed. 1997 Sep. 77(2):F115-8. [Medline].

Watchko JF. Common hematologic problems in the newborn nursery. Pediatr Clin North Am. 2015 Apr. 62 (2):509-24. [Medline].

Taniguchi K, Sumie M, Sugibayashi R, Wada S, Matsuoka K, Sago H. Twin anemia-polycythemia sequence after laser surgery for twin-twin transfusion syndrome and maternal morbidity. Fetal Diagn Ther. 2015. 37 (2):148-53. [Medline].

Sundaram M, Dutta S, Narang A. Fluid Supplementation versus No Fluid Supplementation in Late Preterm and Term Neonates with Asymptomatic Polycythemia: A Randomized Controlled Trial. Indian Pediatr. 2016 Nov 15. 53 (11):983-986. [Medline].

Doshi H, Moradiya Y, Roth P, Blau J. Variables associated with the decreased risk of intraventricular haemorrhage in a large sample of neonates with respiratory distress syndrome. Arch Dis Child Fetal Neonatal Ed. 2016 May. 101 (3):F223-9. [Medline].

Hopewell B, Steiner LA, Ehrenkranz RA, Bizzarro MJ, Gallagher PG. Partial exchange transfusion for polycythemia hyperviscosity syndrome. Am J Perinatol. 2011 Aug. 28 (7):557-64. [Medline].

Jegen Kandasamy, MD Assistant Professor, Department of Pediatrics, Division of Neonatal-Perinatal Medicine, University of Alabama School of Medicine

Jegen Kandasamy, MD is a member of the following medical societies: American Academy of Pediatrics, Indian Academy of Pediatrics, National Neonatology Forum of India

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Brian S Carter, MD, FAAP Professor of Pediatrics, University of Missouri-Kansas City School of Medicine; Attending Physician, Division of Neonatology, Children’s Mercy Hospital and Clinics; Faculty, Children’s Mercy Bioethics Center

Brian S Carter, MD, FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Hospice and Palliative Medicine, American Academy of Pediatrics, American Pediatric Society, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Society for Pediatric Research, National Hospice and Palliative Care Organization

Disclosure: Nothing to disclose.

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Karen J Lessaris, MD Clinical Faculty, Department of Pediatrics, Division of Neonatology, Carolinas Medical Center

Karen J Lessaris, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association

Disclosure: Nothing to disclose.

Scott S MacGilvray, MD Clinical Professor, Department of Pediatrics, Division of Neonatology, The Brody School of Medicine at East Carolina University

Scott S MacGilvray, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Polycythemia of the Newborn

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