Polycythemia of the Newborn Clinical Presentation
- Author: Karen J Lessaris, MD; Chief Editor: Ted Rosenkrantz, MD more...
History
Neonates with polycythemia may have the following findings:
- Lethargy
- Irritability
- Jitteriness
- Tremors
- Seizures
- Cerebrovascular accidents
- Respiratory distress
- Cyanosis
- Apnea
Physical
- General
- The most obvious finding is plethora or ruddiness.
- Priapism may be observed in male patients.
- CNS
- CNS manifestations are the most common problems observed with polycythemia and hyperviscosity.
- Symptoms include lethargy, irritability, jitteriness, tremors, seizures, and cerebrovascular accidents.
- Cardiopulmonary: Manifestations include respiratory distress, tachypnea, cyanosis, apnea, and congestive heart failure. Increases in hematocrit (Hct) are associated with a decrease in pulmonary blood flow in all newborns. In those with a Hct level of 65% or more, the decrease in pulmonary blood flow may be associated with respiratory distress and cyanosis.
- GI
- Poor feeding is reported in more than one half of all infants with polycythemia and hyperviscosity.
- Necrotizing enterocolitis (NEC) is a rare but devastating complication of polycythemia or hyperviscosity. Historically, about 44% of term infants with NEC have polycythemia. More recent data suggest that polycythemia may not have a large role in the development of NEC in the term infant but may be related to partial exchange transfusion (PET) with colloid to reduce the Hct.
- Renal: Manifestations include decreased glomerular filtration rates, oliguria, hematuria, proteinuria, and renal vein thrombosis.
- Metabolic
- Hypoglycemia is the most common metabolic derangement and is observed in 12-40% of infants with polycythemia.
- Hypocalcemia is the next most common metabolic derangement and is found in 1-11% of neonates with polycythemia.
- Coagulation
- Coagulation can be affected.
- Thrombocytopenia may be noted.
- Disseminated intravascular coagulation (DIC) is rare.
Causes
- Increased fetal erythropoiesis secondary to fetal hypoxia. Underlying causes include the following:
- Placental insufficiency can be secondary to preeclampsia, primary renovascular disease, chronic or recurrent abruptio placenta, maternal cyanotic congenital heart disease, postdate pregnancy, and maternal smoking. Most of these maternal conditions may also be associated with intrauterine growth restriction (IUGR).
- Endocrine abnormalities associated with increased fetal oxygen consumption resulting in fetal hypoxia include congenital thyrotoxicosis and Beckwith-Wiedemann syndrome or infants of a diabetic mother (IDM) with poor glycemic control.
- Genetics disorders (eg, trisomy 13, trisomy 18, trisomy 21) are also underlying causes.
- Hypertransfusion
- Delayed cord clamping 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%.
- Gravity also may be a factor because of the position of the delivered infant in relation to the maternal introitus before cord clamping.
- In the event of delayed cord clamping, blood flow to the infant is enhanced by oxytocin.
- Twin-to-twin transfusion syndrome 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.
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