Anemia of prematurity

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

Overview

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 is a normochromic, normocytic anemia commonly seen in premature infants cared for in the neonatal intensive care unit. Normally, all the newborns develop anemia during the first few weeks of their life after birth. Decreased erythropoietin production, increased erythropoietin metabolism, and shortened RBC lifespan leads to anemia in newborns. Term infants tolerate it well and do not require any treatment. This physiological anemia in newborns resolves with increasing age. Whereas, premature infants develop anemia rapidly and more profoundly. Blood loss during phlebotomy and other illness related to prematurity contribute to the development of anemia of prematurity. Severity of symptoms varies with the blood hemoglobin levels. Treatment involves blood transfusion and recombinant human erythropoietin therapy.

Historical perspective

Classification

There is no established system for the classification of anemia of prematurity.

Pathophysiology

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.

Causes

Common causes of anemia of prematurity include preterm birth, blood loss during phlebotomy, increased destruction of red blood cells, and decreased production of red blood cells. Iron, vitamin B6, vitamin E, and folate deficiencies are less common causes of anemia of prematurity.

Differentiating Anemia of prematurity from other diseases

Anemia of prematurity should be differentiated from anemia due to increased red blood cell destruction, increased blood loss, and decreased red blood cell production. It should also be differentiated from other causes of normocytic normochromic anemia.

Epidemiology and Demographics

Age

Anemia of prematurity is a common problem in neonatal intensive care unit (NICU). It usually affects preterm and low birth weight infants born before 32-weeks of gestation. The risk of anemia of prematurity is inversely proportional to birth weight and gestational age at time of birth.

Gender

Men and women are equally likely to develop anemia of prematurity

Race

There is no racial predilection for anemia of prematurity

Risk factors

Anemia of prematurity is a serious problem in preterm infants. Common risk factors in the development of anemia of prematurity are preterm birth, low birth weight, and excess blood loss during phlebotomy. Less common risk factors are family history of anemia, anemia and nutritional deficiencies in mother during pregnancy, multiple gestations, complications during pregnancy and delivery, blood loss during pregnancy and delivery, and twin-to-twin transfusion.

Natural History, Complications, and Prognosis

Anemia of prematurity can be asymptomatic or produce abnormal clinical signs and symptoms depending on the hemoglobin levels. Mild symptoms usually resolve spontaneously without treatment. Severe symptoms require treatment with blood transfusion and erythropoietin. Untreated anemia of prematurity can lead to poor growth, apnea, and cardiovascular instability. The prognosis of anemia of prematurity is good with prompt diagnosis and early treatment.

Diagnosis

History and Symptoms

Majority of patients with anemia of prematurity are either asymptomatic or develop vague and non-specific symptoms. They usually present with pallor and lethargy. Decreased activity, breathing difficulties, feeding difficulties, and difficulty in gaining weight are common symptoms. Less common symptoms are tachycardia, heart murmurs, and metabolic acidosis.

Physical Examination

Patients with anemia of prematurity usually appear pale and lethargic. Physical examination of patients with anemia of prematurity is usually remarkable for pallor, decreased activity, and poor growth.

Laboratory Findings

Laboratory findings consistent with the diagnosis of anemia of prematuriy are reduced hemoglobin, hematocrit, and reticulocyte count in the blood. Normocytic, normochromic RBCs and red blood cell precursors are seen predominantly on the peripheral smear of patients with anemia of prematurity.

Ultrasound

There are no ultrasound findings associated with anemia of prematurity. Cranial USG and abdominal USG can be done to exclude other causes of anemia.

Other Imaging Findings

There are no other imaging findings associated with anemia of prematurity.

Other Diagnostic Studies

There are no other diagnostic studies associated with anemia of prematurity.

Treatment

Medical Therapy

Blood transfusion is the mainstay in the treatment of anemia of prematurity. Treatment of infants with anemia of prematurity depends on the severity of symptoms. Asymptomatic patients are managed with close monitoring and supportive care. Whereas, blood transfusion and recombinant erythropoietin therapy are required to treat infants with symptomatic anemia of prematurity.

Primary Prevention

Effective measures for the primary prevention of anemia of prematurity include limiting blood loss during phlebotomy, cord blood sampling for the laboratory investigations, and improving placental transfusion.

Secondary Prevention

There are no established measures for the secondary prevention of anemia of prematurity.

References

Template:WH Template:WS

Historical Perspective

Please help WikiDoc by adding content here. It’s easy! Click here to learn about editing.

References

Template:WH Template:WS

Classification

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

Overview

There is no established system for the classification of anemia of prematurity.

Classification

There is no established system for the classification of anemia of prematurity.

References

Template:WH Template:WS

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.

Template:WH Template:WS

Causes

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

Overview

Common causes of anemia of prematurity include preterm birth, blood loss during phlebotomy, increased destruction of red blood cells, and decreased production of red blood cells. Iron, vitamin B6, vitamin E, and folate deficiencies are less common causes of anemia of prematurity.

Causes

Life threatening causes

There are no life-threatening causes of anemia of prematurity.

Common causes

Common causes of anemia of prematurity include^[1]:

Premature birth
Phlebotomy for laboratory testing in preterm infants
Increased destruction of RBC
- Shortened lifespan of RBC
- Rh-incompatibility
- Hemolytic anemias
Decreased production of RBC
- Decreased erythropoietin production

Less common causes

Less common causes of anemia of prematurity include^[2]:

Iron, Vitamin B6, Vitamin E, and Folate deficiencies

References

↑ 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”.

Template:WH Template:WS

Differentiating Anemia of prematurity from other Diseases

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 should be differentiated from anemia due to increased red blood cell destruction, increased blood loss, and decreased red blood cell production. It should also be differentiated from other causes of normocytic normochromic anemia.

Differential Diagnosis

Anemia of prematurity should be differentiated from anemia due to increased red blood cell destruction, increased blood loss, and decreased red blood cell production. Anemia of prematurity should also be differentiated from other causes of normocytic normochromic anemia.^[1]

Increased RBC destruction

Anemia of prematurity should be differentiated from anemia due to increased red blood cell destruction:

Decrease RBC production

Anemia of prematurity should be differentiated from anemia due to decreased red blood cell production:

Increase blood loss

Anemia of prematurity should be differentiated from anemia due to increased blood loss:

Normocytic Normochromic anemia

Differentiating Anemia of prematurity from other diseases

Anemia of prematurity must be differentiated based on different laboratory findings including mean cell volume (MCV), reticulocytosis, and hemolysis.

To review the differential diagnosis of anemia, see below table.

Disease	Genetics	Clinical manifestation					Lab findings
		History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Iron studies					Specific finding on blood smear
		History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	Transferrin or TIBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Anemia of prematurity ^[2]	−	Premature birth Low birth weight Phlebotomy NICU admission	Pallor Lethargy Decreased activity	Signs of anemia	−	−	Normochromic	Normocytic	Nl	↓	Nl	Nl	↓	↑	↑	↓	↓↓↓	Predominant red blood cell precursors
Iron deficiency anemia^[3]	−	Menorrhagia GI loss GI surgery Pregnancy	Koilonychia Pica	Glossitis Cheilosis Dysphagia	−	−	Hypochromic	Microcytic	↑	Nl or ↓	Nl	Nl	↓	↑	↑	↓	↓↓↓	Central pallor
Iron deficiency anemia (early phase)^[4]	−	Pica Glossitis Cheilosis	Fatigue Headache	Koilonychia Conjunctival pallor Dry skin	−	−	Normochromic	Normocytic	↑	↓	Nl	Nl	↓	↑	↑	↓	↓	Pencil cells Elliptocytosis Hypochromasia
Lead poisoning^[5]	−	House painted with chipped paint	Burtonian lines Basophilic stippling Wrist drop Foot drop	Wrist drop Foot drop Burtonian lines	−	−	Hypochromic	Microcytic	Nl	Nl or ↓	Nl	Nl	Nl to ↓	Nl	Nl	Nl to ↓	−	RBCs retain aggregates of rRNA Basophilic stippling
Sideroblastic anemia^[6]	Defect in ALA synthase gene Autosomal dominant Autosomal recessive X-linked	Alcohol abuse Isoniazid use Chloramphenicol use Lead poisoning Idiopathic	Seborrheic dermatitis Glossy Tongue Tingling	Patient present with symptoms of Vitamin B6, copper deficiency symptoms	−	−	Hypochromic	Microcytic	Nl	Nl or ↓	Nl	Nl	↑	Nl	Nl to ↓	↑	−	Ringed sideroblasts
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Anemia of chronic disease^[7]	−	Rheumatoid arthritis SLE Neoplasm Chronic kidney disease	Headache Shortness of breath	−	−	−	Hypochromic	Microcytic	Nl	Nl or ↓	Nl	↑	↓	Nl	↓	↑	−	NA
Thalassemia^[8]	α-thalassemia α– globin gene deletions Cis deletions Trans deletions β-thalassemia Point mutation in splice sites and promoter sequences	Associated with parvovirus B19	α-thalassemia Hydrops fetalis β-thalassemia Skeletal deformities Chipmunk facies	Hepatomegaly Splenomegaly	−	−	Hypochromic	Microcytic	Nl	Thalassemia trait: Nl or ↓ Thalassemia Syndromes: ↑	Nl	Nl	Nl to ↑	Nl	Nl	↑	Nl to ↑	Target cells Anisopoikilocytosis
G6PD deficiency^[9]	Defect in G6PD enzyme X-Linked recessive	History of using Sulfa drugs Antimalarials Fava Beans Infections	Back pain Hemoglobinuria	Back pain	+	Intrinsic	Normochromic	Normocytic	↑	↑ but usually causes resolution within 4-7 days	↓	↓	Nl to ↑	Nl	↑	↑	↑	RBC with Heinz bodies Bite cells Blister cells
Pyruvate kinase deficiency^[10]	Mutation in the PKLR and PKM gene Autosomal recessive	Gallstones	Hydrops fetalis Neonatal hyperbilirubinemia Iron overload Perinatal complications	Skin ulcers Splenomegaly	+	Intrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↑	Nl	Nl	↑	−	Prickle cells Polychromatophilic erythrocytes
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Sickle cell anemia^[11]	Hbs point mutation causes a single amino acid replacement in β chain	High altitude Low Oxygen Acidosis African-American race Parvovirus B19 infection	Painful crisis Dactylitis Priapism Acute chest syndrome Avascular Necrosis Stroke Autosplenectomy Salmonella osteomyelitis	Dactylitis Priapism	+	Intrinsic	Normochromic	Normocytic	↑	↑	↓	Nl or moderately ↑	Nl	Nl	Nl or moderately ↑	↓	Nl	Increased erythropoiesis Howell-Jolly bodies Anisocytosis
HbC disease^[12]	Glutamic acid–to-lysine mutation in β-globin	Gallstone	Joint pains Increased risk of infections	Splenomegaly Cholelithiasis Avascular necrosis of the femoral head	+	Intrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	Nl	Nl	Nl	↓	−	Hemoglobin crystals inside RBCs Target cells
Paroxysmal nocturnal hemoglobinuria^[13]^[14]	PIGA gene mutations Impaired synthesis of GPI anchor for decay-accelerating factor	Associated with aplastic anemia Thrombosis	Fatigue Chest pain Dyspnea on exertion Headache	Chronic hemolysis Hepatomegaly Ascites Papilledema Skin nodules	+	Intrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↓	Nl	↑	↓	−	NA
Hereditary spherocytosis^[15]	Mutations in Ankyrin, Band 3, Protein 4.2, and spectrin	Associated with parvovirus B19 Cholelithiasis Megaloblastic crisis	Aplastic crisis	Splenomegaly	+	Intrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↓	Nl	↑	Nl	−	Small, round RBCs with less surface area and no central pallor
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Microangiopathic hemolytic anemia^[16]^[17]	−	Associated with DIC TTP HUS SLE HELLP syndrome Hypertensive emergency	Purpura Confusion Aphasia Diplopia	Numbness of an arm or hand Jaundice Pale conjunctiva	+	Extrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↓	Nl	−	↑	−	Helmet cells
Macroangiopathic hemolytic anemia^[18]	Autoimmune	Associated with Prosthetic heart valves Aortic stenosis	Pallor Fatigue	Signs of anemia Complications of hemolysis Decreased vascular volume	+	Extrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↓	Nl	−	−	−	Spherocytes or schistocytes
Autoimmune hemolytic anemia^[19]	−	Associated with: SLE CLL Mycoplasma pneumonia	Painful blue fingers and toes on exposure to cold temperature Chest pain Chills Dizziness Tachycardia Headache Fatigue	Painful, blue fingers and toes with cold weather	+	Extrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	↓	Nl	−	−	−	RBC agglutination
Aplastic anemia^[20]	Constitutive expression of Tbet Mutations in the perforin gene Mutations in SAP gene	Exposure to Radiation Drugs like Benzene, chloramphenicol, alkylating agents Viral infections like EBV, HIV, Hepatitis Fanconi anemia Idiopathic like Immune mediated, primary stem cell defect	Symptoms based on underlying condition	Short stature Cafe-au-lait spots Thumb defects Radial defects	−	−	Normochromic	Normocytic	↑	↓	Nl	Nl	↓	↓	Nl	↑	↓	Pancytopenia Fatty infiltration
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Folate deficiency^[21]	Impaired DNA synthesis	Alcohol consumption History of using drugs like methotrexate, trimethoprim, and phenytoin Low socioeconomic groups with poor nutrition Older people Pregnant and lactating women	No neurological symptoms vs B12 deficiency Odynophagia Angular stomatitis	Glossitis Signs of heart failure Anencephaly and spina bifida	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	RBC macrocytosis Hypersegmented neutrophils Pancytopenia in severe cases
Vitamin B12 deficiency^[22]	Impaired DNA synthesis	Pernicious anemia Crohn’s disease Gastrectomy Veganism Diphyllobothrium latum infection	Psychosis Insomnia Depression Cognitive slowing Restless leg syndrome	Neurological deficit Myelopathy Memory loss with reduced attention span Nystagmus Positive romberg sign Positive Lhermitte’s sign	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	Senile neutrophil Anisocytosis Ovalocytes
Orotic aciduria^[23]	Autosomal recessive Deficiency of enzyme UMPS	Episodic vomiting Rhabdomyolysis	Coma Gastrointestinal manifestation	Neurological manifestation	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	NA
Fanconi anemia^[24]	Autosomal recessive X-linked recessive	History of anemia at age 16	Hypopigmentation Cafe-au-lait patches Radial ray anomaly	Significant for bilateral short thumbs	−	−	Anisochromic	Macrocytic	↑	↓	Nl	Nl	↑	↑	↓	↑	↑	Nl appearing WBC, RBC and Platelets But the number is greatly reduced
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear
Diamond-Blackfan anemia^[25]	Mutations in: RPL5 RPL11 RPL35A RPS7 RPS10 RPS17 RPS19 RPS24 RPS26	Associated with myelodysplastic syndrome Increased risk of AML	Pale skin Sleepiness Heart murmurs	Triphalangeal thumbs Short stature Microcephaly Hypertelorism Ptosis Micrognathia	−	−	Anisochromic	Macrocytic	Nl	↓	Nl	Nl	↑	↑	↓	↑	↑	NA
Infections^[26]	−	Associated with Malaria Babesia	Fever	Fever Signs of shock Headache	+	Extrinsic	Normochromic	Normocytic	↑	↑	↓	Nl	Nl	Nl	−	−	−	Trophozoite Maltese crosses
Chronic kidney disease^[27]	−	Pericarditis Encephalopathy Rectal incontinence Decreased libido Restless leg syndrome	Polyuria Hematuria Edema	Hypertension	−	−	Normochromic	Normocytic	↑	Nl/↑	Nl	↑	↓	−	↓	↑	↓	Nl
Liver disease^[28]	−	Hepatitis Binge drinking Gall bladder disease	Jaundice Abdominal pain Itchy skin	Ascites Right upper quadrant pain Hepatomegaly Swelling in the legs Ankle swelling	−	−	Anisochromic	Macrocytic	↑	↑	Nl	Nl	↑	↑	↓	↑	↑	Round macrocytes Target macrocytes
Alcoholism^[29]	−	History of increased alcohol intake Folic acid deficiency	Memory impairment Nausea Sweating	Truncal obesity Asterixis Encephalopathy Spider angiomas Hematemesis Gynecomastia	−	−	Anisochromic	Macrocytic	↑	↑	Nl	Nl	↑	↑	↓	↑	↑	Oval macrocytes Hypersegmented neutrophils
Disease	Genetics	History	Symptoms	Signs	Hemolysis	Intrinsic/ Extrinsic	Hb concentration	MCV	RDW	Reticulocytosis	Haptoglobin levels	Hepcidin	Serum iron	Serum Tfr level	IBC	Ferritin	Transferrin saturation	Specific finding on blood smear

References

↑ “www.cancertherapyadvisor.com”.
↑ Strauss RG (November 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.
↑ Camaschella C (May 2015). “Iron-deficiency anemia”. N. Engl. J. Med. 372 (19): 1832–43. doi:10.1056/NEJMra1401038. PMID 25946282.
↑ De Andrade Cairo RC, Rodrigues Silva L, Carneiro Bustani N, Ferreira Marques CD (June 2014). “Iron deficiency anemia in adolescents; a literature review”. Nutr Hosp. 29 (6): 1240–9. doi:10.3305/nh.2014.29.6.7245. PMID 24972460.
↑ Bain BJ (December 2014). “Lead poisoning”. Am. J. Hematol. 89 (12): 1141. doi:10.1002/ajh.23852. PMID 25220013.
↑ Bottomley SS, Fleming MD (August 2014). “Sideroblastic anemia: diagnosis and management”. Hematol. Oncol. Clin. North Am. 28 (4): 653–70, v. doi:10.1016/j.hoc.2014.04.008. PMID 25064706.
↑ Roy CN (2010). “Anemia of inflammation”. Hematology Am Soc Hematol Educ Program. 2010: 276–80. doi:10.1182/asheducation-2010.1.276. PMID 21239806.
↑ Zainal NZ, Alauddin H, Ahmad S, Hussin NH (December 2014). “α-Thalassemia with Haemoglobin Adana mutation: prenatal diagnosis”. Malays J Pathol. 36 (3): 207–11. PMID 25500521.
↑ Luzzatto L, Seneca E (February 2014). “G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications”. Br. J. Haematol. 164 (4): 469–80. doi:10.1111/bjh.12665. PMC 4153881. PMID 24372186.
↑ Grace RF, Zanella A, Neufeld EJ, Morton DH, Eber S, Yaish H, Glader B (September 2015). “Erythrocyte pyruvate kinase deficiency: 2015 status report”. Am. J. Hematol. 90 (9): 825–30. doi:10.1002/ajh.24088. PMC 5053227. PMID 26087744.
↑ Singh PC, Ballas SK (March 2015). “Emerging drugs for sickle cell anemia”. Expert Opin Emerg Drugs. 20 (1): 47–61. doi:10.1517/14728214.2015.985587. PMID 25431087.
↑ Lemonne N, Billaud M, Waltz X, Romana M, Hierso R, Etienne-Julan M, Connes P (2016). “Rheology of red blood cells in patients with HbC disease”. Clin. Hemorheol. Microcirc. 61 (4): 571–7. doi:10.3233/CH-141906. PMID 25335812.
↑ Bunyaratvej A, Butthep P (January 1992). “Cytometric analysis of paroxysmal nocturnal hemoglobinuria erythrocytes”. J Med Assoc Thai. 75 Suppl 1: 237–42. PMID 1402472.
↑ Kahng J, Kim Y, Kim JO, Koh K, Lee JW, Han K (January 2015). “A novel marker for screening paroxysmal nocturnal hemoglobinuria using routine complete blood count and cell population data”. Ann Lab Med. 35 (1): 35–40. doi:10.3343/alm.2015.35.1.35. PMC 4272963. PMID 25553278.
↑ Da Costa L, Galimand J, Fenneteau O, Mohandas N (July 2013). “Hereditary spherocytosis, elliptocytosis, and other red cell membrane disorders”. Blood Rev. 27 (4): 167–78. doi:10.1016/j.blre.2013.04.003. PMID 23664421.
↑ Morishita E (July 2015). “[Diagnosis and treatment of microangiopathic hemolytic anemia]”. Rinsho Ketsueki (in Japanese). 56 (7): 795–806. doi:10.11406/rinketsu.56.795. PMID 26251142.
↑ George JN, Charania RS (March 2013). “Evaluation of patients with microangiopathic hemolytic anemia and thrombocytopenia”. Semin. Thromb. Hemost. 39 (2): 153–60. doi:10.1055/s-0032-1333538. PMID 23390027.
↑ Westphal RG, Azen EA (May 1971). “Macroangiopathic hemolytic anemia due to congenital cardiovascular anomalies”. JAMA. 216 (9): 1477–8. PMID 5108522.
↑ Hill QA (October 2015). “Autoimmune hemolytic anemia”. Hematology. 20 (9): 553–4. doi:10.1179/1024533215Z.000000000401. PMID 26447931.
↑ Dolberg OJ, Levy Y (2014). “Idiopathic aplastic anemia: diagnosis and classification”. Autoimmun Rev. 13 (4–5): 569–73. doi:10.1016/j.autrev.2014.01.014. PMID 24424170.
↑ Koike H, Takahashi M, Ohyama K, Hashimoto R, Kawagashira Y, Iijima M, Katsuno M, Doi H, Tanaka F, Sobue G (March 2015). “Clinicopathologic features of folate-deficiency neuropathy”. Neurology. 84 (10): 1026–33. doi:10.1212/WNL.0000000000001343. PMID 25663227.
↑ Hunt A, Harrington D, Robinson S (September 2014). “Vitamin B12 deficiency”. BMJ. 349: g5226. PMID 25189324.
↑ Grohmann K, Lauffer H, Lauenstein P, Hoffmann GF, Seidlitz G (April 2015). “Hereditary orotic aciduria with epilepsy and without megaloblastic anemia”. Neuropediatrics. 46 (2): 123–5. doi:10.1055/s-0035-1547341. PMID 25757096.
↑ Alter BP (2014). “Fanconi anemia and the development of leukemia”. Best Pract Res Clin Haematol. 27 (3–4): 214–21. doi:10.1016/j.beha.2014.10.002. PMC 4254647. PMID 25455269.
↑ Vlachos A, Blanc L, Lipton JM (June 2014). “Diamond Blackfan anemia: a model for the translational approach to understanding human disease”. Expert Rev Hematol. 7 (3): 359–72. doi:10.1586/17474086.2014.897923. PMID 24665981.
↑ Bustinduy AL, Parraga IM, Thomas CL, Mungai PL, Mutuku F, Muchiri EM, Kitron U, King CH (March 2013). “Impact of polyparasitic infections on anemia and undernutrition among Kenyan children living in a Schistosoma haematobium-endemic area”. Am. J. Trop. Med. Hyg. 88 (3): 433–40. doi:10.4269/ajtmh.12-0552. PMC 3592521. PMID 23324217.
↑ Drawz P, Rahman M (June 2015). “Chronic kidney disease”. Ann. Intern. Med. 162 (11): ITC1–16. doi:10.7326/AITC201506020. PMID 26030647.
↑ Marks PW (July 2013). “Hematologic manifestations of liver disease”. Semin. Hematol. 50 (3): 216–21. doi:10.1053/j.seminhematol.2013.06.003. PMID 23953338.
↑ Yokoyama A, Yokoyama T, Brooks PJ, Mizukami T, Matsui T, Kimura M, Matsushita S, Higuchi S, Maruyama K (May 2014). “Macrocytosis, macrocytic anemia, and genetic polymorphisms of alcohol dehydrogenase-1B and aldehyde dehydrogenase-2 in Japanese alcoholic men”. Alcohol. Clin. Exp. Res. 38 (5): 1237–46. doi:10.1111/acer.12372. PMID 24588059.

Template:WH Template:WS

Epidemiology and Demographics

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 is a common problem in neonatal intensive care unit (NICU). It usually affects preterm and low birth weight infants born before 32-weeks of gestation. The risk of anemia of prematurity is inversely proportional to birth weight and gestational age at time of birth. It affects male and female infants equally with no racial predilection.

Incidence

Anemia of prematurity is a common problem in neonatal intensive care unit (NICU)
Each week, in the United States, 10,000 new cases of premature births are reported^[1]
Extremely low birth weight (ELBW) infants constitute about 6% of the premature births
Approximately, 80-90% of ELBW infants require at least one blood transfusion due to anemia of prematurity

Age

Anemia of prematurity is commonly seen in premature infants born before 32-weeks of gestation^[2]
The risk of anemia of prematurity is inversely proportional to weeks of gestation and weight at the time of birth
Nearly, 50% of ELBW infants and infants born before 29 weeks of gestation require at least one blood transfusion during first two weeks of life. More than 80% of such infants receive additional blood transfusion before getting discharge from hospital^[3]

Gender

The prevalence and incidence of anemia of prematurity do not vary by gender

Race

There is no racial predilection for anemia of prematurity

References

↑ 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”.
↑ 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.

Template:WH Template:WS

Risk Factors

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 is a serious problem in preterm infants. Common risk factors in the development of anemia of prematurity are preterm birth, low birth weight, and excess blood loss during phlebotomy. Less common risk factors are family history of anemia, anemia and nutritional deficiencies in mother during pregnancy, multiple gestations, complications during pregnancy and delivery, blood loss during pregnancy and delivery, and twin-to-twin transfusion.

Risk Factors

Common risk factors

Common risk factors in the development of anemia of prematurity include^[1]^[2]:

Premature birth
Low birth weight
Excess blood loss during phlebotomy for laboratory investigation in preterm infants

Less common risk factors

Less common risk factors in the development of anemia of prematurity include^[3]:

Family history of anemia
Multiple gestations
Anemia during pregnancy
Complications during pregnancy and delivery
Excess blood loss during pregnancy and delivery
Twin-to-twin transfusion
Nutritional deficiency of iron, vitamin B6, and vitamin B12 in mother

References

↑ 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.
↑ 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.
↑ Sekretar LB (1998). “[The risk factors for early anemia in premature infants]”. Lik Sprava (6): 114–7. PMID 9844893.

Template:WH Template:WS

Natural History, Complications and Prognosis

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 can be asymptomatic or produce abnormal clinical signs and symptoms depending on the hemoglobin levels. Mild symptoms usually resolve spontaneously without treatment. Severe symptoms require treatment with blood transfusion and erythropoietin. Untreated anemia of prematurity can lead to poor growth, apnea, and cardiovascular instability. The prognosis of anemia of prematurity is good with prompt diagnosis and early treatment.

Natural History

In preterm infants, anemia gets worsened due to other illness related to prematurity and blood loss during phlebotomy^[1]
Premature infants develop abnormal clinical signs and symptoms depending on the hemoglobin levels^[2]
Some infants can be asymptomatic or develop mild symptoms that require little or no therapy
Others develop severe signs and symptoms that require treatment with blood transfusion and erythropoietin
If left untreated, anemia of prematurity leads to cardiovascular instability

Complications

Anemia of prematurity can develop following complications^[3]:

Complications that can develop as a result of the treatment of anemia of prematurity are^[4]

Infections
Allergic reactions
Iron overload
Fluid overload
Electrolyte imbalance
Calcium disturbance
Immune mediated adverse reactions
Transfusion of toxic substances present in the blood
Necrotizing enterocolitis
Bronchopulmonary dysplasia

Prognosis

The prognosis of anemia of prematurity is good with prompt diagnosis and early treatment^[5]
Milder cases usually resolve spontaneously with age
Without adequate treatment, anemia of prematurity will result in serious complications

References

↑ Strauss RG (November 2010). “Anaemia of prematurity: pathophysiology and treatment”. Blood Rev. 24 (6): 221–5. doi:10.1016/j.blre.2010.08.001. PMID 20817366.
↑ “www.cancertherapyadvisor.com”.
↑ “www.cancertherapyadvisor.com”.
↑ “www.cancertherapyadvisor.com”.
↑ “www.cancertherapyadvisor.com”.

Template:WH Template:WS

Diagnosis

Treatment

Medical Therapy | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case#1

Template:WikiDoc Sources

[pmid6502312-1] 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.

[pmid20817366-2] 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.

[pmid8847295-6] 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”.

[pmid9787158-8] 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.

[pmid20817366-1] 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.

[2] “Anemia of Prematurity | Annual Review of Medicine”.

[1] “www.cancertherapyadvisor.com”.

[2] Strauss RG (November 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.

[pmid25946282-3] Camaschella C (May 2015). “Iron-deficiency anemia”. N. Engl. J. Med. 372 (19): 1832–43. doi:10.1056/NEJMra1401038. PMID 25946282.

[pmid24972460-4] De Andrade Cairo RC, Rodrigues Silva L, Carneiro Bustani N, Ferreira Marques CD (June 2014). “Iron deficiency anemia in adolescents; a literature review”. Nutr Hosp. 29 (6): 1240–9. doi:10.3305/nh.2014.29.6.7245. PMID 24972460.

[pmid25220013-5] Bain BJ (December 2014). “Lead poisoning”. Am. J. Hematol. 89 (12): 1141. doi:10.1002/ajh.23852. PMID 25220013.

[pmid25064706-6] Bottomley SS, Fleming MD (August 2014). “Sideroblastic anemia: diagnosis and management”. Hematol. Oncol. Clin. North Am. 28 (4): 653–70, v. doi:10.1016/j.hoc.2014.04.008. PMID 25064706.

[pmid21239806-7] Roy CN (2010). “Anemia of inflammation”. Hematology Am Soc Hematol Educ Program. 2010: 276–80. doi:10.1182/asheducation-2010.1.276. PMID 21239806.

[pmid25500521-8] Zainal NZ, Alauddin H, Ahmad S, Hussin NH (December 2014). “α-Thalassemia with Haemoglobin Adana mutation: prenatal diagnosis”. Malays J Pathol. 36 (3): 207–11. PMID 25500521.

[pmid24372186-9] Luzzatto L, Seneca E (February 2014). “G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications”. Br. J. Haematol. 164 (4): 469–80. doi:10.1111/bjh.12665. PMC 4153881. PMID 24372186.

[pmid26087744-10] Grace RF, Zanella A, Neufeld EJ, Morton DH, Eber S, Yaish H, Glader B (September 2015). “Erythrocyte pyruvate kinase deficiency: 2015 status report”. Am. J. Hematol. 90 (9): 825–30. doi:10.1002/ajh.24088. PMC 5053227. PMID 26087744.

[pmid25431087-11] Singh PC, Ballas SK (March 2015). “Emerging drugs for sickle cell anemia”. Expert Opin Emerg Drugs. 20 (1): 47–61. doi:10.1517/14728214.2015.985587. PMID 25431087.

[pmid25335812-12] Lemonne N, Billaud M, Waltz X, Romana M, Hierso R, Etienne-Julan M, Connes P (2016). “Rheology of red blood cells in patients with HbC disease”. Clin. Hemorheol. Microcirc. 61 (4): 571–7. doi:10.3233/CH-141906. PMID 25335812.

[pmid1402472-13] Bunyaratvej A, Butthep P (January 1992). “Cytometric analysis of paroxysmal nocturnal hemoglobinuria erythrocytes”. J Med Assoc Thai. 75 Suppl 1: 237–42. PMID 1402472.

[pmid25553278-14] Kahng J, Kim Y, Kim JO, Koh K, Lee JW, Han K (January 2015). “A novel marker for screening paroxysmal nocturnal hemoglobinuria using routine complete blood count and cell population data”. Ann Lab Med. 35 (1): 35–40. doi:10.3343/alm.2015.35.1.35. PMC 4272963. PMID 25553278.

[pmid23664421-15] Da Costa L, Galimand J, Fenneteau O, Mohandas N (July 2013). “Hereditary spherocytosis, elliptocytosis, and other red cell membrane disorders”. Blood Rev. 27 (4): 167–78. doi:10.1016/j.blre.2013.04.003. PMID 23664421.

[pmid26251142-16] Morishita E (July 2015). “[Diagnosis and treatment of microangiopathic hemolytic anemia]”. Rinsho Ketsueki (in Japanese). 56 (7): 795–806. doi:10.11406/rinketsu.56.795. PMID 26251142.

[pmid23390027-17] George JN, Charania RS (March 2013). “Evaluation of patients with microangiopathic hemolytic anemia and thrombocytopenia”. Semin. Thromb. Hemost. 39 (2): 153–60. doi:10.1055/s-0032-1333538. PMID 23390027.

[pmid5108522-18] Westphal RG, Azen EA (May 1971). “Macroangiopathic hemolytic anemia due to congenital cardiovascular anomalies”. JAMA. 216 (9): 1477–8. PMID 5108522.

[pmid26447931-19] Hill QA (October 2015). “Autoimmune hemolytic anemia”. Hematology. 20 (9): 553–4. doi:10.1179/1024533215Z.000000000401. PMID 26447931.

[pmid24424170-20] Dolberg OJ, Levy Y (2014). “Idiopathic aplastic anemia: diagnosis and classification”. Autoimmun Rev. 13 (4–5): 569–73. doi:10.1016/j.autrev.2014.01.014. PMID 24424170.

[pmid25663227-21] Koike H, Takahashi M, Ohyama K, Hashimoto R, Kawagashira Y, Iijima M, Katsuno M, Doi H, Tanaka F, Sobue G (March 2015). “Clinicopathologic features of folate-deficiency neuropathy”. Neurology. 84 (10): 1026–33. doi:10.1212/WNL.0000000000001343. PMID 25663227.

[pmid25189324-22] Hunt A, Harrington D, Robinson S (September 2014). “Vitamin B12 deficiency”. BMJ. 349: g5226. PMID 25189324.

[pmid25757096-23] Grohmann K, Lauffer H, Lauenstein P, Hoffmann GF, Seidlitz G (April 2015). “Hereditary orotic aciduria with epilepsy and without megaloblastic anemia”. Neuropediatrics. 46 (2): 123–5. doi:10.1055/s-0035-1547341. PMID 25757096.

[pmid25455269-24] Alter BP (2014). “Fanconi anemia and the development of leukemia”. Best Pract Res Clin Haematol. 27 (3–4): 214–21. doi:10.1016/j.beha.2014.10.002. PMC 4254647. PMID 25455269.

[pmid24665981-25] Vlachos A, Blanc L, Lipton JM (June 2014). “Diamond Blackfan anemia: a model for the translational approach to understanding human disease”. Expert Rev Hematol. 7 (3): 359–72. doi:10.1586/17474086.2014.897923. PMID 24665981.

[pmid23324217-26] Bustinduy AL, Parraga IM, Thomas CL, Mungai PL, Mutuku F, Muchiri EM, Kitron U, King CH (March 2013). “Impact of polyparasitic infections on anemia and undernutrition among Kenyan children living in a Schistosoma haematobium-endemic area”. Am. J. Trop. Med. Hyg. 88 (3): 433–40. doi:10.4269/ajtmh.12-0552. PMC 3592521. PMID 23324217.

[pmid26030647-27] Drawz P, Rahman M (June 2015). “Chronic kidney disease”. Ann. Intern. Med. 162 (11): ITC1–16. doi:10.7326/AITC201506020. PMID 26030647.

[pmid23953338-28] Marks PW (July 2013). “Hematologic manifestations of liver disease”. Semin. Hematol. 50 (3): 216–21. doi:10.1053/j.seminhematol.2013.06.003. PMID 23953338.

[pmid24588059-29] Yokoyama A, Yokoyama T, Brooks PJ, Mizukami T, Matsui T, Kimura M, Matsushita S, Higuchi S, Maruyama K (May 2014). “Macrocytosis, macrocytic anemia, and genetic polymorphisms of alcohol dehydrogenase-1B and aldehyde dehydrogenase-2 in Japanese alcoholic men”. Alcohol. Clin. Exp. Res. 38 (5): 1237–46. doi:10.1111/acer.12372. PMID 24588059.

[pmid20817366-1] 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.

[2] “Anemia of Prematurity | Annual Review of Medicine”.

[pmid30805447-3] 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.

[pmid20817366-1] 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.

[pmid30805447-2] 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.

[pmid9844893-3] Sekretar LB (1998). “[The risk factors for early anemia in premature infants]”. Lik Sprava (6): 114–7. PMID 9844893.

[1] Strauss RG (November 2010). “Anaemia of prematurity: pathophysiology and treatment”. Blood Rev. 24 (6): 221–5. doi:10.1016/j.blre.2010.08.001. PMID 20817366.

[2] “www.cancertherapyadvisor.com”.

[3] “www.cancertherapyadvisor.com”.

[4] “www.cancertherapyadvisor.com”.

[5] “www.cancertherapyadvisor.com”.

[1]

[2]

[3]

[4]

[5]

[6]

[7]

[8]

[1]

[2]

[1]

[3]

[4]

[5]

[6]

[7]

[8]

[9]

[10]

[11]

[12]

[13]

[14]

[15]

[16]

[17]

[18]

[19]

[20]

[21]

[22]

[23]

[24]

[25]

[26]

[27]

[28]

[29]

[3]

[2]

[3]

Anemia of prematurity

Overview

Historical perspective

Classification

Pathophysiology

Causes

Differentiating Anemia of prematurity from other diseases

Epidemiology and Demographics

Age

Gender

Race

Risk factors

Natural History, Complications, and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

References

References

Overview

Classification

References

Overview

Pathophysiology

Physiological anemia in newborns

Pathological Anemia of Prematurity

References

Overview

Causes

Life threatening causes

Common causes

Less common causes

References

Overview

Differential Diagnosis

Increased RBC destruction

Decrease RBC production

Increase blood loss

Normocytic Normochromic anemia

Differentiating Anemia of prematurity from other diseases

References

Overview

Incidence

Age

Gender

Race

References

Overview

Risk Factors

Common risk factors

Less common risk factors

References

Overview

Natural History

Complications

Prognosis

References

Diagnosis

Treatment

Case Studies

Looking for the patient version?