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{{Anemia of prematurity}}
{{Anemia of prematurity}}


{{CMG}}
{{CMG}}; {{AE}} {{Asra}}


==Overview==
==Overview==
[[Anemia of prematurity]] occurs as a result of a combination of increased [[blood loss]] or [[red blood cell]] destruction, decreased [[erythropoietin]] production, increased [[erythropoietin]] [[metabolism]], deficient [[iron]] stores, and decreased [[RBC]] lifespan. [[Phlebotomy]] is the major contributing factor of [[anemia of prematurity]]. [[Term]] [[infant|infants]] tolerate [[anemia]] well and do not develop any [[symptom|symptoms]] and resolve with increasing age. Whereas, in [[premature birth|preterm]] [[infant|infants]] these factors exaggerate to cause a severe form of [[anemia]] more rapidly.


==Pathophysiology==
==Pathophysiology==
The total volume of blood in premature infants is approximately 100ml/kg of body weight--approximately 5 ounces for a 1.5kg infant.  Blood sampling done for laboratory testing in the first days of life can easily remove enough blood to produce anemia.  As anemia develops, the amount of oxygen delivered by the hemoglobin in the blood to the body organs declines.  Normally this stimulates increased production of[[erythropoietin]] (EPO), but this response is diminished in premature infants.  While the reason for this decreased response is not fully understood, it is theorized that there is a genetically timed switch from [[liver|hepatic]] production of EPO, which occurs in-utero, to[[kidney|renal]] production. Since hepatic production is stimulated by lower levels of oxygen delivery (reflecting the lower levels present in the fetus) and since the red blood cells are carrying higher amounts of oxygen after birth, the level of red blood cells itself must drop significantly before EPO production will begin in premature infants who have not yet switched from hepatic to renal EPO production.  This level may be as low as a [[hemoglobin]] of 6.5g/dL, corresponding to an [[hematocrit]] of approximately 19.
The [[pathogenesis]] of [[anemia of prematurity]] is multifactorial. [[Anemia of prematurity]] is the result of a combination of decreased [[erythropoietin]] production, increased [[erythropoietin]] [[metabolism]], deficient [[iron]] stores, decreased [[RBC]] lifespan, and blood loss during [[phlebotomy]].<ref name="pmid6502312">{{cite journal| author=Stockman JA, Graeber JE, Clark DA, McClellan K, Garcia JF, Kavey RE| title=Anemia of prematurity: determinants of the erythropoietin response. | journal=J Pediatr | year= 1984 | volume= 105 | issue= 5 | pages= 786-92 | pmid=6502312 | doi=10.1016/s0022-3476(84)80308-x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6502312  }} </ref><ref name="pmid20817366">{{cite journal| author=Strauss RG| title=Anaemia of prematurity: pathophysiology and treatment. | journal=Blood Rev | year= 2010 | volume= 24 | issue= 6 | pages= 221-5 | pmid=20817366 | doi=10.1016/j.blre.2010.08.001 | pmc=2981681 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20817366 }} </ref><ref>{{cite web |url=https://doi.org/10.1146/annurev.me.32.020181.001043 |title=Anemia of Prematurity &#124; Annual Review of Medicine |format= |work= |accessdate=}}</ref>
===Physiological anemia in newborns===
Normally, all the [[newborns]] experience a fall in the [[haemoglobin]] concentration during the first few weeks of life. Healthy, [[full-term]] [[infants]] usually develop [[anemia]] around 10-12 weeks of life after birth. [[Hemoglobin]] concentration never falls below 10 g/dl in healthy [[infants]]. [[Physiological anemia]] is well tolerated and does not require any therapy.<ref name="pmid20817366">{{cite journal| author=Strauss RG| title=Anaemia of prematurity: pathophysiology and treatment. | journal=Blood Rev | year= 2010 | volume= 24 | issue= 6 | pages= 221-5 | pmid=20817366 | doi=10.1016/j.blre.2010.08.001 | pmc=2981681 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20817366 }} </ref><ref>{{cite web |url=https://doi.org/10.1146/annurev.me.32.020181.001043 |title=Anemia of Prematurity &#124; Annual Review of Medicine |format= |work= |accessdate=}}</ref><ref>{{cite journal |vauthors=Alan S, Arsan S |title=Prevention of the anaemia of prematurity |journal=Int J Pediatr Adolesc Med |volume=2 |issue=3-4 |pages=99–106 |date=2015 |pmid=30805447 |pmc=6372412 |doi=10.1016/j.ijpam.2015.10.001 |url=}}</ref>
 
*After birth, an [[embryo]] transitions from a [[hypoxic]] state [[in-utero]] to an [[infant]] in a relatively hyperoxic environment
*This transition leads to an increase in [[blood oxygen]] and [[tissue oxygen]] concentration in [[newborns]]
*Increased [[oxygen]] concentration inhibits [[erythropoietin]] production and eventually stops [[erythropoiesis]]
*Due to the rapid growth and disproportionate [[RBC production]], [[hemoglobin]] levels fall gradually in infants
*The drop in [[hemoglobin]] concentration continues until the [[tissue hypoxia]] develops which usually takes around 6-12weeks after birth
*[[Tissue hypoxia]] activates the [[oxygen sensors]] present in the [[kidney]] and [[liver]] to stimulate the [[erythropoietin]] and [[red blood cells]] (RBC) production
*[[Fullterm newborns]] have enough iron stores for [[erythropoiesis]] until 20 weeks of life
*Infants have a shorter [[RBC]] lifespan and increased [[erythropoietin]] [[metabolism]] when compared to adults<ref name="pmid8847295">{{cite journal| author=Widness JA, Veng-Pedersen P, Peters C, Pereira LM, Schmidt RL, Lowe LS| title=Erythropoietin pharmacokinetics in premature infants: developmental, nonlinearity, and treatment effects. | journal=J Appl Physiol (1985) | year= 1996 | volume= 80 | issue= 1 | pages= 140-8 | pmid=8847295 | doi=10.1152/jappl.1996.80.1.140 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8847295 }} </ref>
 
===Pathological Anemia of Prematurity===
In [[preterm]] [[infants]], multiple [[physiological factors]] exaggerate and combine to result in [[pathological anemia]]. [[Hemoglobin]] levels drop rapidly to less than 10 g/dl around 4-6 weeks after birth. [[Infants]] with 1-1.5 kg of [[birthweight]] have [[hemoglobin]] levels around 8 g/dl, whereas [[infants]] with [[birthweight]] less than 1 kg have [[hemoglobin]] levels around 7 g/dl or less. The profound decrease in [[hemoglobin]] levels in [[premature infants]] produce abnormal [[signs]] and [[symptoms]] and require a [[blood transfusion]]. <ref name="pmid20817366">{{cite journal| author=Strauss RG| title=Anaemia of prematurity: pathophysiology and treatment. | journal=Blood Rev | year= 2010 | volume= 24 | issue= 6 | pages= 221-5 | pmid=20817366 | doi=10.1016/j.blre.2010.08.001 | pmc=2981681 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20817366  }} </ref><ref>{{cite web |url=https://doi.org/10.1146/annurev.me.32.020181.001043 |title=Anemia of Prematurity &#124; Annual Review of Medicine |format= |work= |accessdate=}}</ref>
 
*A greater proportion of [[fetal erythropoiesis]] and [[iron transport]] from [[mother]] to [[infants] occur during the [[third trimester]]. So, [[infants]] born [[prematurely]] have deficient [[iron stores]] required for the [[red blood cells production]]
*[[Blood loss]] during [[phlebotomy]] is the major contributor of [[anemia of prematurity]]
*Majority of [[preterm]] [[infants]] are [[sick]] and [[critically ill]] that require frequent [[blood sampling]] for various [[laboratory investigations]] needed for their [[clinical monitoring]]. The average amount of [[blood loss]] during [[sampling]] ranges from 0.8-3.1 ml/kg/day, a significant amount that requires replacement
*[[Preterm]] [[infants]] are at increased risk of [[nosocomial infections]] that lead to [[oxidative hemolysis]]
*In [[premature infants]], [[liver]] is the major site of [[erythropoiesis]]. [[Liver]] [[EPO]] is less sensitive to anemia and tissue hypoxia<ref name="pmid9787158">{{cite journal| author=Dame C, Fahnenstich H, Freitag P, Hofmann D, Abdul-Nour T, Bartmann P | display-authors=etal| title=Erythropoietin mRNA expression in human fetal and neonatal tissue. | journal=Blood | year= 1998 | volume= 92 | issue= 9 | pages= 3218-25 | pmid=9787158 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9787158 }} </ref>
*[[Preterm infants]] have deficient [[Vitamin E]], [[Vitamin B12]], [[Folic acid]] stores required for [[red blood cells]] production
*A combination of [[blood loss]], decreased [[erythropoietin]] production, deficient [[iron stores]], increased [[erythropoietin]] [[metabolism]], shortened [[RBC]] lifespan contribute to the development of [[anemia of prematurity]]
 
==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Latest revision as of 09:47, 12 August 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Asra Firdous, M.B.B.S.[2]

Overview

Anemia of prematurity occurs as a result of a combination of increased blood loss or red blood cell destruction, decreased erythropoietin production, increased erythropoietin metabolism, deficient iron stores, and decreased RBC lifespan. Phlebotomy is the major contributing factor of anemia of prematurity. Term infants tolerate anemia well and do not develop any symptoms and resolve with increasing age. Whereas, in preterm infants these factors exaggerate to cause a severe form of anemia more rapidly.

Pathophysiology

The pathogenesis of anemia of prematurity is multifactorial. Anemia of prematurity is the result of a combination of decreased erythropoietin production, increased erythropoietin metabolism, deficient iron stores, decreased RBC lifespan, and blood loss during phlebotomy.[1][2][3]

Physiological anemia in newborns

Normally, all the newborns experience a fall in the haemoglobin concentration during the first few weeks of life. Healthy, full-term infants usually develop anemia around 10-12 weeks of life after birth. Hemoglobin concentration never falls below 10 g/dl in healthy infants. Physiological anemia is well tolerated and does not require any therapy.[2][4][5]

Pathological Anemia of Prematurity

In preterm infants, multiple physiological factors exaggerate and combine to result in pathological anemia. Hemoglobin levels drop rapidly to less than 10 g/dl around 4-6 weeks after birth. Infants with 1-1.5 kg of birthweight have hemoglobin levels around 8 g/dl, whereas infants with birthweight less than 1 kg have hemoglobin levels around 7 g/dl or less. The profound decrease in hemoglobin levels in premature infants produce abnormal signs and symptoms and require a blood transfusion. [2][7]

References

  1. ↑ Stockman JA, Graeber JE, Clark DA, McClellan K, Garcia JF, Kavey RE (1984). "Anemia of prematurity: determinants of the erythropoietin response". J Pediatr. 105 (5): 786–92. doi:10.1016/s0022-3476(84)80308-x. PMID 6502312.
  2. ↑ 2.0 2.1 2.2 Strauss RG (2010). "Anaemia of prematurity: pathophysiology and treatment". Blood Rev. 24 (6): 221–5. doi:10.1016/j.blre.2010.08.001. PMC 2981681. PMID 20817366.
  3. ↑ "Anemia of Prematurity | Annual Review of Medicine".
  4. ↑ "Anemia of Prematurity | Annual Review of Medicine".
  5. ↑ Alan S, Arsan S (2015). "Prevention of the anaemia of prematurity". Int J Pediatr Adolesc Med. 2 (3–4): 99–106. doi:10.1016/j.ijpam.2015.10.001. PMC 6372412. PMID 30805447.
  6. ↑ Widness JA, Veng-Pedersen P, Peters C, Pereira LM, Schmidt RL, Lowe LS (1996). "Erythropoietin pharmacokinetics in premature infants: developmental, nonlinearity, and treatment effects". J Appl Physiol (1985). 80 (1): 140–8. doi:10.1152/jappl.1996.80.1.140. PMID 8847295.
  7. ↑ "Anemia of Prematurity | Annual Review of Medicine".
  8. ↑ Dame C, Fahnenstich H, Freitag P, Hofmann D, Abdul-Nour T, Bartmann P; et al. (1998). "Erythropoietin mRNA expression in human fetal and neonatal tissue". Blood. 92 (9): 3218–25. PMID 9787158.

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