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Polycythemia
Neonatal polycythemia is defined as a venous hematocrit greater than 65%. It can be normovolemic, hypervolemic, or hypovolemic. Common causes include placental transfusion, maternal conditions like diabetes, and intrauterine hypoxia. Symptoms include poor feeding, lethargy, and cardiac or neurological issues. Screening is recommended for small or large infants and those with risk factors. Management may involve partial exchange transfusion to lower the hematocrit if symptoms are present or it is over 70% without symptoms. Studies found partial exchange transfusion effectively reduces hematocrit but did not find clinical benefits in asymptomatic infants.
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Introduction to neonatal polycythemia, its definition, influencing factors, major causes, effects, complications, and clinical trials regarding management.
Defining neonatal polycythemia with hematocrit criteria, discussing blood viscosity measurement techniques and their implications in clinical settings.
Various factors affecting neonatal hematocrit, including gestational age, placental transfusion timings, and blood sampling considerations.
Classification of polycythemia into normovolemic, hypervolemic, and hypovolemic types with detailed causes related to each.
Consequences of neonatal polycythemia, including hyperviscosity, organ dysfunction, and long-term neurodevelopmental outcomes associated with the condition.
Guidelines for screening neonates for polycythemia, management recommendations, including partial exchange transfusions, emphasizing timely interventions.
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Polycythemia
- 1. Neonatal PolycythemiaDr. vijay Moderator :Dr. Sanjeev
- 2. OBJECTIVES Definition factorsthat potentially influence neonatal hematocrit Major causes of polycythemia Effects (signs and symptoms) and complications Clinical trials that studied the effects of partial exchange transfusion (PET) Recommendations - diagnosis & management of NP
- 3. DEFINITION Neonatal polycythemiadefined in most neonatology textbooks as a venous HCT >65% This cutoff has been chosen based on the observation that blood viscosity exponentially increases above a Hct of 65% or hemoglobin concentration higher than 22.0 g/dl a statistical definition of infants at risk neither based upon the risk for symptoms or for complications
- 5. MEASURE HEMATOCRIT ORBLOOD VISCOSITY? How to define hyperviscosity ? Viscosity depends on Hematocrit, plasma proteins (especially fibrinogen), deformability of erythrocytes, erythrocyte aggregation , interaction of cell components with vessel walls The gold standard - measurement of viscosity is a whole blood viscometer that can accurately measure the viscosity of blood (expressed in centipoise) whole blood viscometers are not universally available Because the erythrocyte number is the most important factor affecting viscosity, measurement of the neonatal Hct has been suggested as the best clinical screening test for identifying infants with presumed hyperviscosity
- 6. factors influence normallyHCT 1. Gestational age HCT increases progressively with increasing gestational age, thus NP may occur at much higher rates in post term than in preterm infants (Due to normal variation of Hct) 2. Degree of placental transfusion At term, the total fetoplacental blood volume is about 115 ml/kg fetal weight, and is distributed in the "normal" full-term infant after birth as approximately 70 ml/kg in the infant, with 45 ml/kg remaining in the placenta. This distribution may vary considerably, as more or less blood may remain in the placenta. The main factors influencing placental transfusion are time of cord clamping, position of the delivered infant in relation to the placenta, onset of respiration, presence or not of intrauterine hypoxia, and presence or not of cord compression
- 9. A. Time ofcord clamping Within 30 to 45 seconds following birth, the umbilical arteries are functionally closed, while blood flow from placenta to fetus through the umbilical vein may continue for a few additional minutes . When the infant is delivered at or below the introitus level, if the cord is not clamped, her/his blood volume will increase in a stepwise manner, reaching 55% additional volume after 3 minutes B. Position of the delivered infant in relation to the placenta In vaginally delivered infants who are kept 50 to 60 cm above the placenta, placental transfusion does not occur (7). In contrast, if they are maintained 40 cm below the placenta, placental transfusion is hastened C. Onset of respiration onset of respiration (through generating a negative intrathoracic pressure and presumably increasing the placental-fetal transfusion process
- 10. Polycythemia Study Level ofEvidence Inclusion/Exclusion Intervention Outcomes Statistics/Notes McDonald & Middleton, 2008 Cochrane Review; Cord clamping effects in mothers and term infants. 11 trials. Term infants >= 37 weeks gestation. Excluded breech presentation & multiple pregnancies. Variable timing of cord clamping in the various trials; 1-5 minutes, cessation of pulsation, after placental descent, etc. Polycythemia, Hgb/Hct (@ birth, 24-48hrs, 2-4 months, 4 months, & 6 months). No statistically significant differences found for polycythemia. Hutton and Hassan, 2007 Meta-analysis (15 controlled trials (8 randomized,7 not randomized) of Late vs Early clamping in full tern neonates 15 controlled trials (1912 newborns). 37 or greater wks. ICC vs. late (at least 2 minutes, as defined by this meta-analysis). Noted increased risk of asymptomatic polycythemia > 65% No treatment was needed for noted asymptomatic polycythemia. Kugelman et al, 2007 RCT. 35 neonates. 24-34 6/7 wks. Exluded: vaginal bleeding (abruption, previa, placental tear), major anomaly, severe IUGR < 3%, MGDM w/ insulin, twin-twin or discordant (>20% wt), maternal drug abuse. Hold baby as low as possible without creating tension on cord (20-30cmbelow vaginal introitus, or below incision if C/S). ICC (5-10”) vs. DCC (30-45”) Primary: Initial Hct, MAP during 1st 24 hours. No significant increase in polycythemia. Ultee et al, 2006 RCT 41 infants, 34 wks to 36 6/7 wks; Caucasian mothers. Excluded DM, GDM, PIH, twins, congenital abnls. Infants placed on mother’s abd at neutral position. ICC < 30 seconds vs. DCC at 3 minutes. Primary: Hct at 1 hour & 10 weeks of life; polycythemia (defined as Hct > 0.7) Hct higher w/ DCC compared to ICC @ 1 hr & 10 wks (P < 0.05) No significant differences found between the two groups in regards to polycythemia. Chaparro et al, 2006 RCT 476 normal birthweight infants between 36-42 weeks gestation. Exclude: multiple gestation, PreE or Eclamp, hemorrhage,placental abnl, Trisomy, congenital abnl, any type of diabetes, HTN, Early (10 seconds; mean < 20”)) vs. DCC (2 minutes; mean > 90”). Timed from delivery of shoulders. Maintained @ level of uterus. Secondary: Percentage of infants w/ capillary Hct > 70% Did not see significantly increased risk of polycythemia Delayed Cord Clamping
- 11. Clinical bottom line:Delayed cord clamping does not increase the risk of polycythemia, especially in preterm neonates. Most studies found no clinically or statistically significant increases in polycythemia for babies who received delayed cord clamping. Studies of term infants were also included; any polycythemia seen in these children was asymptomatic/not clinically significant and required no therapy. cardiopathies, chronic renal dz, + tobacco use, not planning to breastfeed for @ least 6 months. Cernadas et al, 2006 RCT 2 obstetrical units in Argentina. 276 neonates with uneventful pregnancies >= 36 wks. Included those with uneventful cephalic vaginal or C/S delivery, singletons. Excluded if > singleton, complicated course, cliinca ldz (DM, PreE, HTN, etc.), evidence of congenital malformations, IUGR (< 10th %ile). CC within first 15 seconds (group 1; mean 12.7 sec), within 1 minute (group 2; mean 59.8 sec), or at 3 minutes (group 3; mean 169.5 sec). For vaginal deliveries, babies held in mother’s arms. C/S, placed on mother’s lap. Babies received ICC if no spontaneous respiratory effort in first 10 seconds, or if discovered congenital malformation, unexpectedly low birthweight, tight nuchal cord. Primary: Hct at 6hrs of life. Secondary: Hct @ 24 & 48 hrs, bili levels, neonatal morbidity/mortality, maternal hemorrhage/Hct, etc. Prevalence of Hct < 45% significantly less in grps 2&3 vs. 1. Prevalence of Hct > 65% significantly increased in grp 3 (14.1%) vs. grps 1 (4.4%) &2 (5.9%). No babies w/ Hct > 65 were symptomatic. Van Rheenen et al, 2007 RCT. 91 term babies. Exclusions: Twins, history of post-partum hemorrhage, GDM, PreE, placental separation before delivery, C/S, tight nuchal cord necessitating early cutting, need for resuscitation, major congenital anomalies. Vaginal births; held 10 cm below introitus. ICC within 20 seconds (mean 15”) vs. DCC done after cessation of cord pulsation (mean 305 seconds, with SD of 136”). Secondary: Included possible side effects (neonatal polycythemia/hyperviscosity, maternal blood loss, etc.) No statistically significant differences were found. RCT in malaria-endemic area. Partially blinded RCT. Not intention to treat. Ibrahim et al, 2000 RCT 32 infants with bwt 501-1250 grams and gestational ages of 24 to less than 29 weeks. Excluded major congenital anomalies, twin to twin transfusion, maternal diabetes, placenta previa/abruption, or maternal history of drug abuse. DCC (20 seconds). Timing started once baby completely out of birth canal in VD. Held supine at level of introitus. Primary: Initial Hct/Hgb. No polycythemia seen.
- 12. D. Presence ornot of intrauterine hypoxia Acute intrapartum and intrauterine asphyxia can be accompanied by an increase in hematocrit (presumably through increased transcapillary escape of plasma) E. Presence or not of cord compression Because the umbilical vein is more compressible than the umbilical arteries, infants born with a tight nuchal cord may actually have low blood volume at birth F. Dehydration Relative loss of water from body 3. Site of blood sampling Capillary HCT is generally higher than venous HCT which in turn is higher than "central" HCT (from umbilical vein) . Capillary HCT from warmed heels correlates well with venous HCT
- 13. 4. Time ofblood sampling Hematocrit rises from values obtained at birth (from cord venous or arterial sampling) to reach a peak at 2 hours of age, staying at a plateau for 2 additional hours, then decreases to go back to values close to cord blood values by 12 to 18 hours of age.
- 14. CAUSES OF POLYCYTHEMIA Classifiedas Normovolemic hypervolemic Hypovolemic
- 15. 1. Normovolemic Polycythemia conditionwhere normal intravascular volume is present despite an increase in red cell mass. It results from increased RBC production due to placental insufficiency and/or chronic intrauterine hypoxia Intrauterine Growth Restriction Maternal Pregnancy Induced Hypertension Discordant Twins Maternal Diabetes Mellitus Prolonged Intrauterine Tobacco Exposure Postmaturity
- 16. 2. Hypervolemic polycythemia occurswhen higher than average blood volume is accompanied by an increased red cell mass acute transfusion to the fetus such as maternal-fetal transfusion twin-to-twin transfusion 3. Hypovolemic polycythemia occurs secondary to a relative increase in number of erythrocytes to plasma volume intravascular dehydration
- 17.
- 18. A. Hyperviscosity leads toa reduction in cerebral blood flow decreased blood flow to the brain→ decrease supply to the brain of other substances carried by plasma, such as glucose, amino acids B. Decreased cerebral blood flow glucose delivery and utilization in the brain decreases C. Increased cellular breakdown of the increased red cell mass Increased breakdown of red cells in NP may be a significant contributing factor of neonatal hyperbilirubinemia D. Hemodynamic effects of hypervolemia or of hypovolemia hypervolemia may lead to congestive heart failure, pulmonary edema, and cardiorespiratory failure hypovolemia can lead to hypoxic-ischemic injury to vital organs.
- 19. A. Central nervoussystem (CNS). Poor feeding, lethargy, hypotonia, apnea, tremors, jitteriness, seizures, cerebral venous thrombosis. B. Cardiorespiratory. Cyanosis, tachypnea, heart murmur, congestive heart failure, cardiomegaly, devated pulmonary vascular resistance, prominent vascular markings on chest x-ray.
- 20. C. Renal. Decreased glomerularfiltration, decreased sodium excretion, renal vein thrombosis, hematuria, proteinuria. D. Other. thrombocytopenia, poor feeding, increased jaundice, persistent hypoglycemia, hypocalcemia, testicular infarcts, necrotizing enterocolitis (NEC), priapism, disseminated intravascular coagulation.
- 21. The long-term neurodevelopmentaloutcome controversial. higher risk for development delays Speech and fine motor abnormalities lower spelling and arithmetic achievement test results and gross motor skills
- 22. Indications for polycythemiascreening Do not routinely screen well term newborns for this syndrome, because there are few data showing that treatment of asymptomatic patients with partial exchange transfusion is beneficial in the long term Small for gestational age (SGA) neonates Large for gestational age (LGA) neonates Infants of diabetic mothers (IDM) Newborns with morphological features of growth restriction Monochorionic twins especially the recipient twin
- 23. How to screen Hematocritat 2nd- 4th HOL Hematocrit > 65% Hematocrit < 65%. No symptoms No further evaluation With symptoms Without symptoms PET repeat -12 & 24 HOL
- 24.
- 25. A. Once othercauses of illness have been considered and excluded (e.g., sepsis, pneumonia, hypoglycemia), any child with symptoms that could be due to hyperviscosity should be considered for partial exchange transfusion if the peripheral venous hematocrit is >65%. B. Asymptomatic infants with a peripheral venous hematocrit between 60% and 70% can usually be managed by increasing fluid intake and repeating the hematocrit in 4 to 6 hours.
- 26. C. exchange transfusionwhen the peripheral venous hematocrit is >70% in the absence of symptoms, but this is a controversial D. The following formula can be used to calculate the exchange with normal saline that will bring the hematocrit to 50% to 60%. In infants with polycythemia, the blood volume varies inversely with the birth weight
- 27. TECHNICAL ASPECTS OFPET Which Diluting Fluid Should Be Used? Plasma, 5% Albumin, Ns, Or Ringer Solution PET Is Efficient In Relieving Immediate Symptoms And Reducing HCT. It Did Not Find Clinically Differences Thus NS Is The Optimal Fluid (Cheapest, With Less Potential Side-effects)
- 28. How much toexchange? Aim for a target, post PET HCT of 55%
- 29. CONCLUSIONS 1. PCTis a venous hematocrit of at least 65%. Such a number is much more likely to be significant in an infant >6 hours than it is at 2-4 hours of age. 2. Symptoms/complications of polycythemia are unlikely to be related to a hematocrit of < 65%. 3. The need for PET and its efficacy have not been demonstrated when PET was conducted after 6 hours of life in asymptomatic infants (regardless of their hematocrit). There is no evidence that PET alters the neurologic or developmental outcomes of asymptomatic polycythemic neonates.
- 30. Outcome of PET Polycythemia Hyperviscosity Chonicintrauterine hypoxia Chronic uterine hypoxia + polycythemia PET will help PET will not help PET partially helps
- 31. Malan et al 1980 RCT, 49 neonates Venous HCT>65 No or mild symps o PET> 12 hrs o Follow up at 8 mo No Diff Goldberg et al 1982 RCT, 20 neonates Capillary HCT>68% + presence of hyperviscosity on venous blood nil symp o PET was performed at > 12 hrs o Follow up at 8 mo No diff Black's et al 1985 RCT, 93 neonates heel stick screening HCT > 65%, a repeat venous HCT>65%, and a venous blood viscosity increased, all neonates o PET performed at 8- 12 hrs o Follow up at 2 yrs o addnl follow up at 7 yrs No diff in mental delay rate, motor delay improved Bada et al 1992 RCT, 28 neonates cord blood HCT>57+ arterial blood HCT >62%+ presence of hyperviscosity o PET at >6hrs(av 10 hrs) o Follow up at 2 yrs No diff in MDI and IQ
- 32. The clinical trialsconducted to date do not allow to reach a practical conclusion, because of the following inherent flaws in design: 1) CNS "damage" may have already occurred before PET was conducted, because PET was performed too late. 2) Confounding variables that may have affected the outcome (such as number of IDM’s, infants of pre eclamptic mothers, smokers, intrauterine growth restriction (IUGR), in whom CNS “damage” may have occurred in utero, unrelated to the polycythemia), were not taken into account in any study 3) the small sample size of all studies 4) follow up of infants was very partial, and did not included all of them. Thus this working group concludes that PET performed after 6 hours of life (after the peak hematocrit/viscosity) is not likely to significantly alter the neurologic or developmental outcomes of asymptomatic polycythemic neonates 5) the effect of PET in symptomatic infants has not been systematically studied
- 33. RECOMMENDATIONS 1. Routinescreening for polycythemia is not recommended. 2. Routine performance of PET in asymptomatic infants is not recommended. 3. Screening for symptoms should be performed carefully and documented in all infants with polycythemia. 4. Normality of blood glucose should be documented in all infants found to have polycythemia. 5. PET causes a prompt relief of symptoms. the presence of symptoms (or of hypoglycemia) should lead to perform PET
- 34. 6. PETshould be performed as early as possible whenever symptoms are present, in view of the potential for more severe symptoms and complications to develop. Before proceeding with PET, it appears that there is a need for thorough, timely, clinical and physical assessment of the newborn. 7. If performed, PET should be done with normal saline.