Renal failure. Renal blood flow is normal. As noted above, plasma volume is reduced. This results in a lower GFR. As such, urine output may be reduced and BUN and creatinine elevated. Necrotizing enterocolitis. There is no evidence that polycythemia or hyperviscosity have a role in the development of necrotizing enterocolitis. However the perinatal events that result in polycythemia are also risk factors for necrotizing enterocolitis.
Therapy for polycythemia partial exchange transfusion may lead to the development of necrotizing enterocolitis as noted below. Imaging studies are not needed for the diagnosis or care of the infant with polycythemia. They may be needed for the infant with polycythemia and an associated problem such as respiratory distress or necrotizing enterocolitis. Obtain a hematocrit in the infant who is at risk as described above. If the blood sample was not from a large, free flowing vessel, then obtain such a sample for confirmation.
The need for appropriate sampling has been discussed above. If one only obtains a capillary sample for diagnosis, then infants with a normal hematocrit will be inappropriately diagnosed as having polycythemia and potentially have unnecessary therapy. Screening hematocrits on all newborn infants was once an accepted practice. This is no longer appropriate due to the low yield and limited number of infants who will need any intervention should the hematocrit be found to be elevated.
The treatment for polycythemia is a partial exchange transfusion PET to lower the hematocrit. Note that all three solutions are equivalent for reducing the hematocrit and blood viscosity.
However, saline is cheaper and does not pose any infectious risk. Fresh frozen plasma FFP should be avoided as it has been associated with the development of necrotizing enterocolitis in this population.
The exchange transfusion should be performed in a sterile manner using the umbilical vein similar to the technique for the classic exchange transfusion for hyperbilirubinema except that the transfused solution is saline, not blood. Supportive therapy should be provided until the PET is performed.
This would include appropriate respiratory support for infant in infant with respiratory distress or provision of intravenous glucose solution for hypoglycemia. PET should not be routinely used. Most infants with polycythemia are asymptomatic and require no therapy. Therapy is reserved for the infant whose symptoms are directly related to the increased hematocrit and blood viscosity. This includes:. Respiratory distress and cyanosis related to changes in pulmonary blood flow and pressure PPHN.
Hypoglycemia that is not responding to usual provision of intravenous dextrose and other causes of hypoglycemia have been excluded. PET should not be performed solely based on the hematocrit alone. It should not be used with the expectation of preventing or improving neurologic function, gastrointestinal function or prevention of NEC. There is no evidence that it will improve the short or long term function of either the brain or GI tract. Provision of intravenous fluids to dilute or lower the hematocrit has not been shown to be effective.
Some affected infants are IUGR. They may have a decreased body water content but the intravascular volume is normal. This type of staged provision of therapy is not based on clinical outcomes in randomized clinical trials or known pathophysiology.
There is no need for any type of long term treatment. Whether the infant is treated with PET or observed, the hematocrit will become lower over time. The polycythemia is an acute problem of the newborn and will not recur unless the child develops some other non-related illness that causes elevation of the hematocrit such dehydration or polycythemia vera in adulthood.
Children with polycythemia, especially those who had evidence of fetal distress in the perinatal period, should have close neurologic follow up as they are at risk for developmental delay and neurologic dysfunction. This risk is not changed by PET.
In discussions with the family of the infant, it is important to discuss what is known about polycythemia and its affect on their newborn. If one discusses possible concerns that are not backed by evidence, that should be made clear.
Important points to share with the family include:. Polycythemia is associated with changes in organ blood flow. However some of these changes are a physiologic response to the elevated HCT and not associated with short or long term organ dysfunction while others may cause acute problems in the newborn period. As reviewed above polycythemia is associated with acute and long term neurologic dysfunction but is not causative. The brain dysfunction appears to be related to perinatal events that directly cause brain injury as well as an elevation in the HCT.
However the vast majority of the newborns will have normal brain function and neurodevelopment. Once these problems are resolved by the PET, there should not be any long term problems.
The family should know what problems the infant is having and whether or not supportive therapy or PET is the most appropriate therapy. They should be made aware of the risk of PET as described above but that these complications are very rare. It is at the higher range in infants born at higher elevations, likely due to the lower partial pressure of oxygen with higher elevation, resulting in lower PaO2 in the mother and fetus. Polycythemia develops in the fetus as reviewed below.
It appears to be due to chronic hypoxia and associated elevated erythropoietin. As reviewed above, the underlying problems in prenatal or perinatal period responsible for polycythemia may be classified into two general categories.
The first is chronic elevation of erythropoietin secondary to chronic fetal hypoxia or genetic syndrome. The second is an acute transfusion of blood either from the placenta due to acute hypoxia or delayed cord clamping or stripping of the cord towards the newborn prior to clamping of the cord. Polycythemia may be associated with conditions that cause chronic intrauterine hypoxemia as outlined above.
In these situations polycythemia in the newborn is an incidental condition and requires no preventive management in and of itself.
Polycythemia in association with maternal diabetes may be prevented by rigorous maternal glycemic control. Avoidance of delayed cord clamping or stripping of the umbilical cord will prevent polycythemia in those infants with normal intrauterine hematocrits. Other causes including chronic intrauterine hypoxia secondary to placental dysfunction as seen in preeclampsia , fetal trisomy or twin to twin transfusion syndrome are not preventable. Rosenkrantz, TS.
Seminars in Thrombosis and Hemostasis.. Sarkar, S, Rosenkrantz, TS. Seminars in Fetal and Neonatal Medicine. Oh, W, Lind, J. Acta Paediatr Scand. Ann Paediatr. Am J Obstet Gynecol.
J Lab Clin Med. J Clin Invest. Fahraeus, R, Lindqvist, T. Am J Physiol. J Appl Physiol. When older infants or young children have seizures, they often To diagnose polycythemia, the newborn gets a blood test. If the results of the blood test indicate the newborn has too many red blood cells, the newborn may be treated for polycythemia. Dehydration occurs when there is significant loss of body water and, to varying amounts, electrolytes This procedure, called partial exchange transfusion, dilutes the remaining red blood cells and corrects the polycythemia.
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Common Health Topics. Blood Problems in Newborns. Test your knowledge. More Content. Polycythemia in the Newborn By Andrew W. The diagnosis is based on a test that measures the amount of red blood cells in the blood. Blood test. Fluids by vein. Was This Page Helpful? Yes No. Overview of Bone Disorders in Children. Anemia in the Newborn.
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