Anemia in pregnancy

Article written and reviewed by Dr Luca Moretti

Anemia in pregnancy is one of the most frequent and clinically important conditions in obstetric practice worldwide, with a significant impact on both maternal and fetal health. According to the World Health Organization, anemia in pregnancy is defined by a hemoglobin concentration below 11 g/dL in the first and third trimesters or below 10.5 g/dL in the second trimester, reflecting physiological adaptation but also the possible presence of nutritional deficiencies, chronic disease or underlying hematological complications.

Pregnancy is associated with profound changes in maternal hematological physiology: increased plasma volume, relative hemodilution, growing requirements for iron, folate and vitamin B12, and changes in red blood cell metabolism make pregnant women particularly vulnerable to anemia. According to WHO estimates, in 2023 anemia affected approximately 35.5% of pregnant women worldwide, with marked differences among regions and socioeconomic groups.

Anemia in pregnancy is not merely a laboratory finding. It is associated with increased risks of preterm birth, low birth weight and other adverse maternal and fetal outcomes, especially in moderate to severe forms; the magnitude of association and the causal relationship depend on cause, severity and clinical context. Understanding the pathophysiological basis, classification, diagnostic sequence and prevention and treatment strategies is essential to reduce its public health impact and improve maternal and infant prognosis.

Physiology of hematopoiesis and hematologic requirements during pregnancy

A full understanding of the pathogenesis and management of anemia in pregnancy requires consideration of the profound changes in maternal hematopoiesis that occur during gestation. Pregnancy induces a progressive increase in plasma volume, by approximately 29% by the end of the second trimester and by an average of 40 to 50% near term. This phenomenon, caused by increased sodium and water retention and hormonal stimulation by progesterone, estrogens and human placental lactogen, is accompanied by a more modest increase in red blood cell mass, approximately 20 to 30%, producing physiological dilution of hemoglobin and hematocrit known as physiological anemia of pregnancy.

Total iron requirements increase considerably during gestation and reach approximately 1000 mg: 300 mg are needed for fetal and placental development, 500 mg for expansion of maternal red blood cell mass and at least 200 mg to compensate for physiological losses. Requirements for folate, needed for DNA synthesis and cellular growth, and vitamin B12, required for nucleoprotein and red blood cell metabolism, also rise, making pregnant women particularly susceptible to nutritional deficiencies, especially when diet is inadequate, pregnancies are closely spaced or malabsorption is present.

Iron homeostasis in pregnancy is regulated by a complex interaction among intestinal absorption, transferrin-mediated transport and mobilization of hepatic stores. Production of hepcidin, the key hormone regulating iron metabolism, is physiologically reduced during pregnancy, thereby increasing intestinal absorption, but this compensation may be insufficient when initial stores are low or blood loss is increased. The erythropoietic response to iron or folate deficiency may also be inhibited or limited by chronic infection, systemic inflammation or associated renal disease.

Although these physiological adaptations support maternal and fetal metabolic requirements, they also create conditions that favor anemia when iron, folate or vitamin B12 intake and stores are inadequate or when pathological conditions impair red blood cell production or survival.

Classification and Epidemiology

Anemia in pregnancy comprises a heterogeneous group of conditions classified according to morphological, etiological and clinical severity criteria. Classification helps distinguish physiological anemia of pregnancy from true pathological states and guides differential diagnosis and treatment.

Morphologically, anemia in pregnancy is divided into:

• Microcytic anemia: characterized by small red blood cells and frequently caused by iron deficiency, although microcytosis is not diagnostic of iron deficiency and may also result from hemoglobinopathies, particularly thalassemias, or more rarely from other conditions.
• Normocytic anemia: characterized by normally sized red blood cells and typical of physiological hemodilution, chronic disease or renal failure.
• Macrocytic anemia: characterized by enlarged red blood cells and generally caused by folate deficiency or vitamin B12 deficiency, conditions that are not uncommon during pregnancy, particularly in women with a poor diet or associated gastrointestinal disease.

From an etiological perspective, iron deficiency is by far the most frequent cause of anemia in pregnancy, accounting for a predominant but population-dependent proportion of cases, followed by folate or vitamin B12 deficiency, inherited hemoglobinopathies, anemia of chronic disease, acute or chronic blood loss and, less commonly, aplastic or autoimmune forms. Several conditions may coexist in the same patient, particularly in settings with a high prevalence of malnutrition, chronic infections or genetic disorders.

According to WHO estimates, approximately 35.5% of pregnant women worldwide in 2023 had anemia, with the greatest burden particularly in Africa and Southeast Asia. Prevalence remains significant even in industrialized countries, ranging from 5% to 20%, especially among socioeconomically disadvantaged groups, ethnic minorities, women with multiple or closely spaced pregnancies and women with preexisting chronic conditions.

Anemia in pregnancy, especially when moderate or severe, is associated with a higher risk of adverse maternal and fetal outcomes, including preterm birth, low birth weight and growth restriction; the strength of association and causality vary with cause, severity and clinical context. Early diagnosis, prevention and correction of nutritional deficiencies are therefore global public health priorities.

Etiology and risk factors

Anemia in pregnancy is a distinct clinical entity whose etiopathogenic mechanisms and predisposing factors are profoundly influenced by gestation. Pregnancy imposes unique hematologic adaptations that affect both the development of anemia and the maternal and fetal response to reduced blood oxygen-carrying capacity.

The central mechanism distinguishing pregnancy-associated anemia from other forms is the progressive increase in plasma volume, which reaches an average increase of approximately 29% by the end of the second trimester and a peak near 48% at term relative to prepregnancy values. This produces marked physiological hemodilution and a relative reduction in hemoglobin and hematocrit. Although part of normal gestational adaptation, this process may conceal pathological anemia or increase its severity. At the same time, fetal and placental growth causes an increase in requirements for iron, folate and vitamin B12, as well as protein and other micronutrients essential for erythropoiesis.

In this setting, the causes of anemia in pregnancy interact with gestation-specific risk factors:

• Pregnancy-related iron deficiency: total iron requirements may reach 1000 mg over the course of gestation. Prepregnancy stores, often already reduced by heavy menstruation, closely spaced pregnancies or chronic malnutrition, may be insufficient to meet maternal and fetal requirements, particularly during the third trimester, when intestinal absorption cannot fully compensate for increased demand.
• Folate deficiency: accelerated nucleic acid synthesis and fetal growth increase folate requirements. Deficiency is more frequent in settings with inadequate intake or without appropriate fortification and is generally less common in high-income countries; it may cause megaloblastic anemia, while inadequate folate status during the periconceptional period increases the risk of neural tube defects.
• Vitamin B12 deficiency: women following vegetarian or vegan diets are at particular risk, as are women with atrophic gastritis, malabsorption, intestinal parasitic infections or use of drugs that interfere with vitamin absorption or metabolism.
• Occult or overt blood loss: previous uterine hemorrhage, gastrointestinal bleeding, hemorrhoids or preexisting gynecological disease may contribute to depletion of iron and erythropoietic resources.
• Increased consumption or reduced nutritional intake: twin or multiple pregnancy, closely spaced pregnancies, adolescent pregnancy, obesity, socioeconomic disadvantage, hyperemesis gravidarum, restrictive diets and eating disorders expose women to multiple deficiencies.
• Chronic infection or inflammation: malaria, intestinal parasitosis, recurrent urinary tract infection and other inflammatory conditions may, through different mechanisms, cause hemolysis, blood loss or functional iron sequestration and reduce erythropoiesis, increasing susceptibility to anemia during pregnancy.
• Inherited disorders: women with thalassemia, sickle cell disease or other hemoglobinopathies may have or develop anemia during pregnancy; isolated sickle cell trait, by contrast, does not usually cause chronic anemia.

Additional risk factors of particular importance include:

• Adolescent pregnancy (10 to 19 years), because maternal growth and gestation create concurrent nutritional requirements, with particular vulnerability at younger ages
• A history of multiple pregnancies, recurrent miscarriage or closely spaced deliveries
• Low educational attainment, economic hardship and linguistic or cultural barriers that limit access to screening and supplementation
• Difficulty accessing healthcare, lack of regular hematologic monitoring and poor adherence to preventive treatment
• Chronic maternal comorbidities, including renal failure, diabetes and immune or autoimmune disease

These frequently coexisting factors create a distinctive vulnerability to anemia in pregnant women and increase the risk of obstetric and neonatal complications compared with the general population.

The physiology of pregnancy may amplify the impact of preexisting or progressive nutritional deficiencies. A fall in hemoglobin may be underestimated because it overlaps with physiological hemodilution and may progress to severe anemia with reduced maternal reserve and association with adverse maternal and fetal outcomes; these outcomes also depend on the cause and clinical context.

Pathogenesis and Pathophysiology

The pathophysiology of anemia in pregnancy is closely linked to the distinctive maternal adaptations and fetal requirements of gestation. Unlike the nonpregnant state, red blood cell metabolism, micronutrient balance and maternal hemodynamic regulation undergo profound changes that are partly physiological and partly potentially pathological.

The first key mechanism is the progressive increase in maternal plasma volume, which reaches its maximum during the third trimester, near term. This expansion is essential for adequate uteroplacental perfusion but is faster and more pronounced than the increase in red blood cell mass, which averages 20 to 30%, producing true hemodilutional anemia. Although physiological, this phenomenon lowers the apparent hemoglobin value and may conceal or worsen latent deficiency.

Metabolically, pregnancy creates an exceptionally high iron requirement to support maternal red blood cell production, fetal and placental growth and formation of fetal hepatic iron stores. Placental iron transport is an active, prioritized process regulated by specific proteins, including ferroportin, transferrin and placental receptors, which favor fetal availability even at the mother's expense but cannot guarantee it in the presence of marked maternal deficiency. When dietary intake and stores are insufficient, progressive iron depletion develops, impairing hemoglobin synthesis and tissue oxygenation.

Folate deficiency, which is also common during pregnancy because of increased nucleotide-synthesis requirements, interferes with erythroblast maturation and DNA synthesis and causes megaloblastic anemia that may coexist with or add to iron deficiency. Vitamin B12 deficiency is less common but may worsen the picture and may also affect myelination of the fetal nervous system.

Anemia secondary to hemoglobinopathies or chronic disease, including renal or inflammatory disease, may first become apparent or may worsen because of increased red blood cell turnover, reduced red blood cell survival and greater maternal and fetal oxygen requirements.

The final effect of these converging mechanisms is reduced maternal blood oxygen-carrying capacity. In response, cardiovascular adaptations develop, including increased cardiac output, tachycardia and peripheral vasodilation. When anemia exceeds compensatory capacity, tissue hypoxia, risk of organ injury and impaired fetal growth may emerge. Severe anemia reduces maternal physiologic reserve and may precipitate heart failure; anemia and iron deficiency are also associated, with variable strength and possible confounding, with preterm birth, low birth weight and greater maternal and neonatal morbidity.

Moderate or severe maternal anemia is associated with intrauterine growth restriction, low birth weight and other adverse fetal outcomes, with variable causality according to etiology and severity. Folate deficiency increases the risk of neural tube defects; associations of vitamin B12 deficiency with congenital defects are not equivalent or universally causal. Maternal iron deficiency may reduce neonatal iron stores.

In summary, the pathophysiology of anemia in pregnancy reflects a complex interaction between physiological maternal adaptations, including hemodilution, increased erythropoietic activity and higher micronutrient requirements, and pathological factors, including nutritional deficiencies, chronic diseases and hemoglobinopathies, with multisystem consequences for maternal, fetal and neonatal health.

Clinical Manifestations

The clinical presentation of anemia in pregnancy is highly variable and is determined by the severity and speed of the fall in hemoglobin, the nature of the underlying deficiency and maternal cardiovascular adaptation. Unlike anemia outside pregnancy, symptoms may be insidious and masked by normal gestational changes, requiring continuous clinical and laboratory surveillance even in the absence of obvious signs.

In the early phase, anemia often causes subtle and nonspecific symptoms such as weakness, easy fatigability, mild tachycardia, palpitations and exertional dyspnea. These symptoms are easily attributed to pregnancy itself and tend to be underestimated by both the patient and healthcare professionals, risking delayed diagnosis until more advanced stages.

As deficiency progresses, clinical signs become more apparent. Skin and mucosal pallor, particularly of the conjunctivae and lips, is a classic but relatively insensitive sign. Increasing tachycardia, dyspnea at rest and difficulty concentrating may precede more severe hemodynamic decompensation, especially in women with preexisting cardiovascular disease or twin pregnancy.

More characteristic manifestations of chronic iron deficiency include brittle nails, atrophic glossitis, angular cheilitis and, in advanced cases, pica. Folate or vitamin B12 deficiency may be associated with erythematous glossitis; neurocognitive changes, paresthesias and ataxia are characteristic mainly of vitamin B12 deficiency, not isolated folate deficiency.

Pregnancy itself amplifies the systemic effects of anemia:

• Infections: risk depends mainly on nutritional deficiencies, comorbidities and associated obstetric conditions; anemia does not itself cause universal immune impairment
• Delayed wound healing and reduced clinical tolerance of postpartum hemorrhage, especially if anemia is not corrected before delivery
• Increased obstetric morbidity, including risk of placental abruption, preterm birth and intrauterine growth restriction

Maternal anemia, especially when moderate or severe, is associated with low birth weight, preterm birth and other adverse neonatal outcomes, but magnitude and causality depend on cause and clinical context. Folate deficiency increases the risk of neural tube defects; vitamin B12 deficiency is associated with some adverse outcomes but should not automatically be equated with folate deficiency. Maternal iron deficiency may also reduce neonatal iron stores.

Severe unrecognized anemia, especially where access to care is limited, may precipitate acute heart failure, reduce tolerance of blood loss and is associated with increased maternal and perinatal risk; hypovolemic shock, when present, is caused by acute loss of blood volume. These complications are rare in countries with advanced obstetric care but remain a major cause of mortality in resource-limited settings.

Prompt diagnosis and assessment of clinical severity are therefore essential to prevent complications and ensure favorable outcomes for both mother and infant.

Investigations and Diagnosis

The diagnosis of anemia in pregnancy requires a systematic and integrated approach that considers the physiological thresholds of gestation and the many potentially overlapping causes. The diagnostic pathway aims not only to recognize anemia early, but also to identify its specific cause and assess maternal and fetal risk so that appropriate treatment and prevention can be instituted.

Clinical suspicion often arises from nonspecific symptoms or abnormalities detected during routine hematologic screening. During pregnancy, screening should be performed according to the applicable guidelines; British guidelines, for example, recommend a complete blood count at the first visit and at 28 weeks, with additional testing according to risk factors and results.

A complete blood count is the first and most important diagnostic test. The definition of anemia in pregnancy is based on trimester-specific hemoglobin thresholds, <11 g/dL in the first and third trimesters and <10.5 g/dL in the second trimester according to the WHO, with allowance for physiological hemodilution. Red blood cell indices, including MCV, MCH, RDW and red blood cell count, help distinguish microcytic anemia caused by iron deficiency, normocytic anemia associated with chronic disease or acute bleeding and macrocytic anemia caused by folate or vitamin B12 deficiency.

A peripheral blood smear allows evaluation of red blood cell morphology and recognition of findings suggestive of specific deficiencies, including microcytosis, hypochromia and anisopoikilocytosis in iron deficiency and macro-ovalocytes and neutrophil hypersegmentation in folate and vitamin B12 deficiency. It also helps identify schistocytes, circulating erythroblasts and other morphological findings compatible with hemolysis; a normal smear alone does not exclude a hemolytic process.

Assessment of iron metabolism, including serum iron, ferritin, transferrin and transferrin saturation, is essential for diagnosing iron-deficiency anemia. A ferritin concentration <30 ng/mL is considered the most sensitive and specific marker of iron depletion during pregnancy. Ferritin is an acute-phase protein, however, and may be falsely normal or elevated during infection or chronic inflammation; in these cases, transferrin saturation and other iron indices, together with the clinical picture, may help establish the diagnosis.

Serum folate and vitamin B12 should be measured in macrocytic anemia, in women with specific risk factors such as vegetarian diets, previous gastrectomy or chronic intestinal disease, or when suggestive neurological signs are present. In selected situations, homocysteine and methylmalonic acid may also be useful to confirm functional deficiency.

When the clinical and laboratory picture indicates, investigations should be extended to include:

• Reticulocyte count to assess the erythropoietic response and distinguish hyporegenerative from regenerative anemia
• Testing for hemoglobinopathies, including electrophoresis and HPLC, in women with microcytosis not explained by iron deficiency, a family history of anemia or origin from areas with a high prevalence of thalassemia, sickle cell disease or other hemoglobinopathies
• Inflammatory markers, including ESR and CRP, to document an inflammatory context and contribute, together with iron studies, reticulocyte count, renal function and the clinical picture, to assessment of possible anemia of inflammation
• Investigation for parasitic infection, chronic infection and renal or hepatic disease when anemia is resistant to replacement therapy

The differential diagnosis must exclude nondeficiency causes, including hemoglobinopathies, anemia of chronic disease, autoimmune hemolysis and bone marrow disorders, particularly when anemia does not respond to standard supplementation or is unexpectedly severe. A detailed medical history, including diet, previous disease, medication use and obstetric history, is essential to define individual risk and plan personalized care.

Finally, in severe anemia with hemoglobin <7 g/dL, signs of maternal decompensation or significant comorbidity, urgent maternal assessment is required; ECG and echocardiography are indicated when suggested by the cardiovascular presentation. Cardiotocographic monitoring and obstetric ultrasound should be performed according to gestational age, maternal severity and specific obstetric indications, not automatically for every case of severe anemia.

In summary, diagnosis of anemia in pregnancy is based on a rational sequence:

• Scheduled periodic hematologic screening for all pregnant women
• Characterization of the type and severity of anemia with complete blood count, peripheral smear, ferritin and vitamin-deficiency markers
• Etiological investigation directed by individual and contextual risk factors
• Continuous monitoring for maternal and fetal complications

This approach enables early diagnosis and optimal management of the individual patient and also helps prevent severe forms and their complications at the population level.

Treatment and prognosis

Management of anemia in pregnancy requires an integrated, multidisciplinary and individualized approach that considers severity, the underlying cause, gestational age and any maternal or fetal comorbidities. The primary objective is prompt correction of the hemoglobin deficit to prevent obstetric and neonatal complications, ensure optimal fetal growth and reduce maternal morbidity.

Primary prevention is a cornerstone of treatment. Folic acid is recommended from the preconception period to prevent neural tube defects, while the WHO recommends daily iron and folic acid supplementation during pregnancy. Standard supplementation includes:

• Elemental iron: 30 to 60 mg daily by mouth, with higher doses in populations at risk of deficiency, multiple pregnancy or low prepregnancy iron stores
• Folic acid: at least 400 micrograms daily, ideally beginning at least one month before conception and continuing throughout pregnancy; prevention of neural tube defects depends mainly on periconceptional and first-trimester intake

Prophylaxis should be individualized according to hematological findings, dietary habits and individual risk, with higher doses or prolonged treatment in particularly vulnerable situations.

When iron-deficiency anemia is confirmed, iron replacement is first-line treatment. Oral iron, preferably ferrous sulfate, fumarate or gluconate, is effective in most cases, but gastrointestinal tolerability and adherence may be limited by adverse effects such as nausea, constipation and dyspepsia. In cases of intolerance, malabsorption, severe anemia or a need for rapid hemoglobin recovery, for example late in the third trimester, intravenous iron may be indicated, generally after the first trimester, according to clinical assessment and the product information for the preparation.

Correction of vitamin deficiencies, including folate and vitamin B12 deficiency, is essential in macrocytic anemia and when requirements are increased or intake or absorption is reduced. Treatment consists of folate, 5 mg daily when deficiency or increased risk is documented, and vitamin B12 orally or intramuscularly according to the cause, with periodic monitoring of hematological response and any neurological effects.

Blood transfusion is reserved for selected situations: severe anemia, especially when delivery is imminent, severe acute hemorrhage or risk of further bleeding, or significantly symptomatic anemia with hemodynamic or cardiac compromise. Fetal distress requires urgent obstetric assessment but is not, by itself, an indication for maternal transfusion. The decision to transfuse must be carefully weighed against the risks of alloimmunization, transmission of infection and circulatory overload, with monitoring appropriate to the clinical context.

Management of secondary causes of anemia, including hemoglobinopathies, chronic infection and renal or inflammatory disease, requires integrated specialist care, targeted treatment of the underlying disorder and close monitoring of maternal and fetal wellbeing.

Regular follow-up with complete blood counts and iron studies is essential to assess response and prevent recurrence; fetal growth monitoring follows obstetric indications and the maternal and fetal risk profile. Health education, adherence to supplementation and a balanced diet rich in heme iron, including red meat and fish, nonheme iron, including legumes, leafy green vegetables and whole grains, and vitamins C, B12 and folate complete treatment and prevention.

Prognosis is closely related to early diagnosis and adequate treatment. In countries with high-quality obstetric care, timely correction of deficiencies treats the hematological deficit and may reduce some adverse outcomes, although the magnitude of benefit depends on cause, severity, timing and care setting. In resource-limited settings, anemia in pregnancy remains an important factor associated with morbidity and mortality, especially where screening, supplementation and follow-up programs are lacking.

In summary, treatment of anemia in pregnancy should be individualized, dynamic and centered on prevention, early diagnosis and targeted correction of deficiency in order to ensure optimal outcomes for mother and infant and reduce the global burden of disease in obstetric populations.

Complications

The complications associated with anemia in pregnancy contribute to maternal and perinatal morbidity, especially where access to obstetric care is limited. Observed associations depend on anemia severity and cause and do not imply direct causality for every outcome.

The most frequent and important maternal complications include:

• Maternal infections: some nutritional deficiencies and conditions causing anemia may be associated with increased infection risk, but anemia is not an independent and universal cause
• Reduced tolerance of hemorrhagic stress: anemia lowers maternal physiologic reserve and worsens tolerance of hypoxia and blood loss; hypovolemic shock instead depends on the magnitude of volume loss, especially postpartum
• Heart failure: severe anemia or preexisting heart disease may cause acute failure, generalized edema and progressive dyspnea because of the increased cardiac workload
• Delayed wound healing and chronic fatigue, with a greater risk of postpartum depression and prolonged hospitalization

Obstetric complications include:

• Placental abruption: an epidemiological association with maternal anemia has been described, without demonstration of a single causal mechanism
• Preterm birth and premature rupture of membranes: these outcomes are associated mainly with more severe anemia and coexisting causal conditions; causality is not uniform
• Increased incidence of postpartum hemorrhage, with a possible need for transfusion and emergency intervention

The main fetal and neonatal complications associated with maternal anemia are:

• Intrauterine growth restriction and low birth weight, associated mainly with moderate to severe anemia and the underlying nutritional or pathological conditions
• Fetal distress in severe or rapidly evolving maternal cases, to be assessed within the overall obstetric context
• Prematurity, associated with short- and long-term consequences, including respiratory problems, infections and neurological abnormalities
• Neural tube defects when folate intake is insufficient; observational associations have been described for vitamin B12, but causality is less well defined
• Reduced neonatal iron stores, with possible predisposition to iron deficiency and anemia during infancy

Transfusion complications, including alloimmunization, transmission of infectious agents and hemolytic reactions, are rare but possible when repeated blood transfusions are required, especially in women who have received multiple transfusions or have rare antigens.

Finally, psychosocial complications, including anxiety, depression and social isolation, are often underestimated but may adversely affect treatment adherence, quality of life and the mother-infant relationship, particularly in high-risk pregnancies or when antenatal care is inadequate.

Prevention, early identification and prompt management of anemia in pregnancy are therefore essential to reduce the burden of complications and improve maternal and infant outcomes worldwide.

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