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Neonatal Polycythemia and Hyperviscosity Seminars in Fetal & Neonatal Medicine (2008) 13, 248e255 available at www.sciencedirect.com journal homepage: www.elsevier.com/locate/siny Neonatal polycythemia and hyperviscosity Shikha Sarkar, Ted S. Rosenkrantz* Department of Pediatrics, Division of NeonatalePerinatal Medicine, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA KEYWORDS Summary Neonatal polycythemia and hyperviscosity are defined as a hematocrit 65% and Hyperviscosity; a viscosity value >2 standard deviations greater than the norm. Although polycythemia can re- Organ blood flow; flect normal fetal adaptation, it has been thought to be responsible for abnormalities in the Partial exchange neonate. Polycythemia and hyperviscosity are associated with blood-flow changes in some or- transfusion; gans, which alter their function. Partial exchange transfusion (PET) has been used to treat both Polycythemia symptomatic and asymptomatic patients. At present, no data support the use of PET in asymp- tomatic infants; the potential benefit in symptomatic infants depends on the symptoms. Stud- ies of long-term neurodevelopmental status do not show any clear long-term benefits for PET. Crystalloids are as effective as colloids in PET and have the advantage of being cheaper and more readily available; also, they do not confer any risk of infection or anaphylaxis. ª 2008 Elsevier Ltd. All rights reserved. Introduction The following is a review of the alterations in physiology and organ function in newborn infants with polycythemia Polycythemia of the neonate was first mentioned in the Bible and hyperviscosity, clinical correlations, and recommenda- (Genesis 25:25). In the 1970s, there were a number of case tions about potential therapies for these infants. reports and small series of infants with symptoms that were thought to be secondary to an elevated hematocrit and blood Incidence viscosity.1e3 This was followed by clinical studies of larger populations of infants, with the emphasis on polycythemia The incidence of polycythemia and hyperviscosity at sea and cerebral function. In the 1980s, several investigators ex- level is 1e2%, whereas at 1600 ft (430 m) it has been shown amined the relationship between polycythemia, hyperviscos- to be 5%.4 Infants who experience chronic or acute fetal ity, and organ system dysfunction, which helped delineate hypoxia have a higher incidence. Premature infants less the changes in organ function as a result of increases in he- than 34 weeks’ gestation rarely have polycythemia or matocrit, viscosity, and arterial oxygen content. hyperviscosity. The measured values for hematocrit and viscosity are affected by a number of factors. Capillary and peripheral vein sources with poor flow overestimate the hematocrit. * Corresponding author. Tel.: þ18606793105;fax:þ1 860 679 Samples of blood from a free-flowing or central source will 1403. yield a true value. They are also affected by the timing at E-mail address: [email protected] (T.S. Rosenkrantz). which it is drawn after birth. Finally, the hematocrit is 1744-165X/$ - see front matter ª 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.siny.2008.02.003 Neonatal polycythemia and hyperviscosity 249 affected by the technique used for analysis, spun is higher but more accurate than automated. Definitions Polycythemia and hyperviscosity are not synonymous terms. Both values vary depending on the source of blood (umbilical vein, peripheral vein, or capillary sample), age of the infant at the time of measurement and the methodology of processing the blood.5 Most researchers define neonatal polycythemia as a he- matocrit 65% when obtained from a large, freely flowing peripheral vein. Gross et al. defined hyperviscosity as a value that was 2 standard deviations greater than the mean6; Ramamurthy and Brans defined hyperviscosity as 3 standard deviations from the mean for blood obtained from three different sites (peripheral vein, capillary, and umbilical vein).5 This coincided with an umbilical venous hematocrit value of 63%. Ramamurthy and Brans found that the capillary values were higher than the peripheral Figure 1 The shaded area represents the viscosity of cord vein values, which were higher than the umbilical vein blood, at shear rates from 2 to 212 sÀ1, for 102 healthy, full- values. term AGA infants (mean Æ 2 standard deviations). Viscosity Polycythemia occurs as a result of increased red cell for 18 ‘symptomatic’ infants is plotted at shear rates of mass, with a decreased, normal, or increased plasma 11 sÀ1 and 106 sÀ1. Hematocrit (Hct) values for each group 7 e volume. The hematocrit peaks at 4 6 h of life, then drops are indicated. Note that the viscosity values increase with e slowly over the next 12 18 h and, by 24 h, it has become higher hematocrit values and with lower shear rates (from similar to the value at birth; thereafter it stays relatively Ref. 6, with permission). stable.8 These changes are caused by transudation of fluid out of the intravascular space. It is important to understand the physics of the flow of fluids to understand how blood viscosity affects blood flow Hematocrit in the newborn infant.9 Viscosity, as defined by Poiseuille, is the ratio of shear stress to shear rate: The hematocrit has a logarithmic relationship with blood viscosity at different shear rates. The most significant ðp À p0Þr 4p shear stress hZ Z changes take place at the lowest shear rates and at 8lQ shear rate hematocrits that exceed 65% (see Fig. 1). where h Z is blood viscosity (dynes/s per square centime- ter or poise), (p À p0) Z pressure gradient across the blood Plasma proteins vessel, r Z radius, l Z length of the blood vessel, and Q Z blood flow. Plasma viscosity (1.0e1.5 centipoise (cP)) is similar to that The shear stress represents the pressure gradient of water and could be considered a Newtonian fluid under along the blood vessel expressed in dynes.10 The shear normal conditions. It does not contribute significantly to rate represents the velocity between the two fluid planes the blood viscosity of the newborn. It may be a problem divided by the distance between them, expressed as per in adults with hyperproteinemic states such as Walden- second (sÀ1). In homogeneous, or Newtonian fluids viscos- strom’s macroglobulinemia. ity remains constant even as shear stress and shear rate change. Blood, being a suspension of particles, does not Red blood cell deformability behave as a Newtonian fluid. The viscosity of blood does not remain constant with variations in the shear RBCs contribute significantly to blood viscosity, both be- stress and shear rate (Fig. 1). The shear rates in large cause they are the most prominent particle suspended in À1 vessels, such as the aorta, are greater (100e300 s ) the blood and because of their intrinsic properties. RBCs À1 than those observed in the arterioles (11e25 s ). Thus consist of a membrane surrounding an internal body of the viscosity in the aorta would be lower than the fluid. RBCs in newborns have a greater degree of deform- arterioles. ability than adult RBCs. The viscosity of internal fluid increases with increasing cell age and also decreasing shear Factors that affect blood viscosity rate. Although a number of factors affect the viscosity of the White blood cells blood, the hematocrit, i.e. the concentration of red blood cells (RBCs), is the primary determinant in the newborn White blood cells (WBCs) are larger than RBCs; they are also infant. less deformable. However, WBCs do not affect blood 250 S. Sarkar, T.S. Rosenkrantz viscosity unless their number significantly exceeds the This phenomenon, referred to as ‘bolus flow’, reflects high normal count, such as in congenital leukemia. hemodynamic efficiency.11 Thus, the hematocrit does not affect blood viscosity at the capillary level (Fig. 2). Fibrinogen Clinical etiologies of polycythemia Fibrinogen contributes little to blood viscosity as it is and hyperviscosity normally low in the newborn. Platelets Erythropoiesis in the human fetus varies with the arterial oxygen content (CaO2) of the blood delivered to the kidney. Decreased oxygen delivery to the kidney results in increased Although the platelets are inflexible, under normal condi- erythropoietin production and release by the fetal kidney. tions they do not contribute much to blood viscosity. They Circulating erythropoietin stimulates the production of can affect blood viscosity in adults with conditions such as RBCs. The endpoint is sufficient oxygen-carrying capacity vaso-occlusive disease, as platelet aggregates will increase and delivery to keep the fetus well oxygenated. The three blood viscosity in small or narrow vessels. common mechanisms of polycythemia are reviewed below. Blood pH Chronic fetal hypoxia Blood viscosity increases with acidosis. At a blood pH < 7 A host of fetal and intrauterine factors can lead to chronic fluid enters the RBCs and alters their shape. This phenom- fetal hypoxia, and in turn result in increased fetal eryth- enon might play an important role in increasing the viscos- ropoiesis, RBC mass, hematocrit, and blood viscosity. The ity in neonates with birth asphyxia. increase in RBC mass compensates for the low partial pressure of oxygen (P O ) of the fetus resulting in a normal Blood vessel size a 2 CaO2 and tissue oxygenation. Pregnancy-related conditions associated with chronic fetal hypoxia include maternal dia- In large blood vessels like the aorta, the blood flow and the betes, pregnancy-induced hypertension, fetal hyperthy- À1 shear rate (100e300 s ) are high compared with the arteri- roidism, and maternal smoking. À1 oles (11e25 s ). Thus, the viscosity in the aorta is lower Maternal diabetes is associated with an increased risk of than the arterioles. This does not apply to capillaries ranging intrauterine hypoxia. These neonates have a high preva- in diameter from 3 to 5 mm. Fahraeus and Lindqvist showed lence of polycythemia, elevated erythropoietin levels, and that viscosity decreases with decreasing size of capillaries.
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