Background: Polycythemia, defined as a venous hematocrit (Hct) of greater than 65%, is a relatively common disorder. The primary concern with polycythemia is related to hyperviscosity and its associated complications. Blood viscosity increases exponentially as the Hct rises above 42%. This associated hyperviscosity is thought to contribute to the symptom complex observed in approximately one half of infants with polycythemia. However, only 47% of infants with polycythemia have hyperviscosity, and only 24% of infants with hyperviscosity have a diagnosis of polycythemia.
Pathophysiology: As the central Hct increases, viscosity increases, resulting in abnormal blood flow kinetics. This condition manifests as poor flow or sludging of blood, which predisposes the infant to microthrombi and decreased tissue oxygenation.
Many factors determine blood viscosity. As previously mentioned, viscosity increases as Hct rises. Plasma volume, plasma proteins, platelets, and endothelial factors also contribute to viscosity. Factors unique to the neonate (eg, increased RBC volume, decreased deformability of the fetal erythrocyte) also contribute to increased viscosity.
Frequency:
* In the US: Polycythemia occurs in 0.4-12% of neonates. 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). However, most infants with polycythemia are of appropriate size or weight for their gestational age (AGA). Infants of mothers with diabetes have an incidence of >40%, and those born to mothers with gestational diabetes have an incidence of >30%. Hyperviscosity occurs in 6.7% of infants.
Mortality/Morbidity:
* The central nervous, cardiopulmonary, gastrointestinal, and renal systems are at risk.
* Metabolic derangements are common.
* Coagulation also can be affected.
Age:
* The Hct peaks 2 hours after birth and then declines until the infant is aged 6 hours, at which time it equals the Hct in cord blood.
* Fewer than 40% of infants with a Hct greater than 64% at 2 hours still have a high value at 12 hours or later.
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History: Neonates with polycythemia may have the following findings:
* Lethargy
* Irritability
* Jitteriness
* Tremors
* Seizures
* Cerebrovascular accidents
* Respiratory distress
* Cyanosis
* Apnea
Physical:
* General
o The most obvious finding is plethora or ruddiness.
o Evaluate the infant for dehydration (eg, sunken fontanelle, dry mucous membranes).
o Priapism may be observed in male patients.
* Central nervous system
o CNS manifestations are the most common problems observed with polycythemia and hyperviscosity.
o Symptoms include lethargy, irritability, jitteriness, tremors, seizures, and cerebrovascular accidents.
* Cardiopulmonary: Manifestations include respiratory distress, tachypnea, cyanosis, apnea, and congestive heart failure.
* Gastrointestinal
o Poor feeding is reported in more than one half of all infants with polycythemia and hyperviscosity.
o 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.
* Renal: Manifestations include decreased glomerular filtration rates, oliguria, hematuria, proteinuria, and renal vein thrombosis.
* Metabolic
o Metabolic alterations are frequent.
o Hypoglycemia is the most common metabolic derangement and is observed in 12-40% of infants with polycythemia.
o Hypocalcemia is the next most common metabolic derangement and is found in 1-11% of neonates with polycythemia.
* Coagulation
o Coagulation can be affected.
o Thrombocytopenia may occur secondary to consumption with thrombosis.
o Disseminated intravascular coagulation (DIC) is rare.
Causes:
* Increased fetal erythropoiesis secondary to fetal hypoxia
o Placental insufficiency can be secondary to preeclampsia, eclampsia, primary renovascular disease, chronic or recurrent abruptio placenta, cyanotic congenital heart disease, postdate pregnancy, maternal smoking, or intrauterine growth restriction (IUGR).
o Endocrine abnormalities secondary to increased oxygen consumption resulting in fetal hypoxia may be due to congenital thyrotoxicosis, congenital adrenal hyperplasia, Beckwith-Wiedemann syndrome, or being the infant of a diabetic mother (IDM).
o Genetics disorders (eg, trisomy 13, trisomy 18, trisomy 21) also may cause in utero hypoxia.
* Hypertransfusion
o 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%.
o Gravity also may be a factor because of the position of the delivered infant in relation to the maternal introitus before cord clamping.
o In the event of delayed cord clamping, blood flow to the infant is enhanced by oxytocin.
o Twin-to-twin transfusion syndrome due to a vascular communication occurs in approximately 10% of monozygotic twin pregnancies.
o Maternal-fetal transfusion may occur.
o As a result of intrapartum asphyxia, the direction of blood flow in the umbilical cord tends to be toward the fetus.
* Dehydration may be due to decreased plasma volume in relation to RBC mass.
2007-02-14 11:13:50
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answer #1
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answered by Dr.Qutub 7
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Sorry chameleon,I think you are confuse with secondary polycythemia.Here is talking about polycthemia vera,It is the disease of chronic myeloproliferative disorder of unknown cause characterized by an increase in hb concentration and red cell number.I only can guss that diabetic mother could carry some genetic defect may some how give to her baby in other way.Since polysythemia vera has unknown cause,talking about the relation to diabetic mother has no point.
2007-02-14 03:24:15
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answer #4
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answered by brother3 4
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hypoxia, in other words lack of enough oxygen going to the baby. When there isn't enough oxygen going to the baby, the baby's metabolism increases the number of red blood cells that carry the oxygen.. so that what little oxygen is available can be carried to tissues more efficiently (and nothing is wasted)..
As far as i understand this is a temporary thing and is seen often (30-40% of diabetic mothers), and unless there is a genetic problem with the baby, this would go away quickly.
2007-02-14 00:03:56
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answer #5
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answered by chameleonGA 4
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2016-05-01 18:06:37
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answer #8
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answered by ? 3
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