Anemia of prematurity pathophysiology
|
Anemia of prematurity Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Anemia of prematurity pathophysiology On the Web |
|
American Roentgen Ray Society Images of Anemia of prematurity pathophysiology |
|
Risk calculators and risk factors for Anemia of prematurity pathophysiology |
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]
- 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[6]
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]
- 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[8]
- 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
- ↑ 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.
- ↑ 2.0 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.
- ↑ "Anemia of Prematurity | Annual Review of Medicine".
- ↑ "Anemia of Prematurity | Annual Review of Medicine".
- ↑ 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.
- ↑ 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.
- ↑ "Anemia of Prematurity | Annual Review of Medicine".
- ↑ 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.