Anemia of prematurity

Introduction to anemia in premature infants The average hemoglobin value of cord blood in premature infants is 175g/L±16g/L (17.5g/dl±1.6g/dl), which is similar to that of term infants. Hemoglobin decreases rapidly in the short term after birth. The premature infants born with a body weight of 1.2-2.5 kg have a hemoglobin value of 80-100 g/L (8.0-10.0 g/dl) at 5-10 weeks after birth, and premature infants with a birth weight of 1.2 kg or less. After 4 to 8 weeks, the hemoglobin value is 65 to 90 g/L (6.5 to 9.0 g/dl). Premature infants with anemia, such as asymptomatic, eat well, gain weight, some people call it physiological anemia in premature infants, no treatment. However, because the mechanism of physiological anemia in premature infants is not exactly the same as that in term infants, and symptoms often appear, some people think that it should be non-physiological and need intervention. basic knowledge Sickness ratio: 0.5% Susceptible people: premature infants Mode of infection: non-infectious Complications: neonatal apnea

Causes of anemia in premature infants

Physiological factors (30%):

It may be shorter than the lifespan of red blood cells in premature infants; rapid growth, expansion of plasma volume, leading to blood dilution; low levels of erythropoietin may be a disorder of gene expression regulation, or may be caused by low sensitivity of target cells .

Pathological factors (20%):

In addition to the above physiological reasons, it may be related to the following factors: 1 nutritional factors; 2 disease factors; 3 iatrogenic blood loss, such as premature infants with a body weight of 1.5kg, total blood volume of about 150ml, blood volume such as accumulation of 7.5 ~ 15ml The blood loss is 5% to 10% of the total blood volume, and 1 kg of the blood drawn by the infant is equivalent to 70 ml of blood drawn by an adult.

Pathogenesis

Physiological factor

(1) Erythropoietin: The erythropoietin produced by the external position of the kidney is not sensitive to the hypoxic environment secondary to anemia. The site of erythropoietin production at birth is transferred from the extrarenal (mostly in the liver) to the kidney. In premature infants, This transfer delay causes a further decrease in hemoglobin.

Low levels of erythropoietin may be a disorder of gene expression regulation, or may be caused by low sensitivity of target cells.

(2) Rapid growth: the plasma volume expands, leading to blood thinning.

(3) The number of red blood cells is small: the average number of red blood cells per kilogram of body weight at birth is lower than that of full-term children.

(4) Low oxygen consumption: The oxygen consumption of premature infants is less than that of full-term children. Their low oxygen demand allows for low oxygen carrying capacity in anemia.

(5) Short life of red blood cells: The amount of vitamin E stored in the body of premature infants is small, and lasts for 2 to 3 months after birth. When vitamin E is deficient, the lipid peroxide of erythrocyte membrane damages the membrane and shortens the life of red blood cells. .

2. Pathological factors

(1) Nutritional factors: Insufficient nutrient reserves before birth, lack of nutrition due to poor sucking and digestion after birth.

1 Iron: For each stage of pregnancy, the fetal iron storage rate is approximately proportional to its weight gain, so the entire fetus maintains a constant iron content of 75 mg/kg and exists in three forms, namely hemoglobin iron, tissue iron and storage. Iron, in anemia-free infants, 75% of total iron is stored as hemoglobin iron, 1g of hemoglobin contains 3.4mg of elemental iron, and infants with low red blood cell count at birth have low iron storage and determine post-natal hematological status. In 1400g premature infants, the study of bone marrow susceptibility to iron found that less iron was found at birth, and hemosiderin could not be seen in the bone marrow by week 8; while bone marrow iron was stored in full-term children for 20 to 24 weeks. Therefore, premature infants appear earlier than full-term iron deficiency.

2 Copper: The storage of copper in the liver of the fetus increases in the last 12 weeks of pregnancy. Therefore, there is often copper deficiency in premature infants. More than 90% of the copper in the plasma is combined with ceruloplasmin under normal conditions, which can promote the absorption and storage of iron. Iron release, copper deficiency can also produce hypochromic small cell anemia with neutropenia.

3 Vitamin E: It is an anti-oxidant, which is very important to maintain the integrity of erythrocyte membrane. The serum value of the baby at birth is 7.2~16.8mol/L, which is 1/3~1/2 of the vitamin E value of the mother. The smaller the deficiency, the lower the vitamin E storage of the baby with a birth weight of 3500g is 20mg, while the birth weight is 1000g, the storage is only 3mg.

4 folic acid: neonatal serum folic acid level is 2 to 3 times higher than that of adults. Due to rapid growth and high metabolic activity, the requirement is 4 to 10 times that of adults, and often falls to the lack of range within 3 to 4 weeks after birth. The decline is faster, because the liver storage is only 159mg, while the full-term infant is 224g, the premature infant <1500g, the serum folic acid reduction leads to the incidence of "folate deficiency" 10% to 30%, within 3 months after birth See megaloblastic anemia.

(2) Disease factors: The disease causes insufficient intake and increased consumption.

(3) iatrogenic blood loss: iatrogenic blood loss for low birth weight children, the amount is relatively large, which indicates that premature infants are prone to early iron deficiency, such as premature infants weighing 1500g, total blood volume is about 150ml, pumping If the amount of blood reaches 7.5 to 15 ml, the blood loss is 5% to 10%, and 1 ml of 1000 g of infant blood is equivalent to 70 ml of blood drawn by an adult.

Premature infant anemia prevention

1. Prenatal gestational-maternal blood loss (the most common type of fetal blood loss) Fetal-fetal transfusion, the etiology and mechanism are not clear, found that amniocentesis, external reversal, intravenous oxytocin and pregnancy-induced hypertension syndrome Occurrence, in addition to active prevention and treatment of pregnancy-induced hypertension syndrome, other operations should be cautious, and pay attention to identify the occurrence of this disease, and take effective diagnosis and treatment measures. If the fetal-fetal transfusion can be diagnosed before delivery, the fetal fetus can be used to relieve symptoms and treat the cause.

2. Loss of blood at birth and postpartum should improve delivery technology, strengthen perinatal care, prevent dystocia and premature delivery, and routinely supplement vitamin K after birth are effective measures.

3. Strengthen the health care during pregnancy and perinatal period, balance the diet of pregnant mother and mother, prevent the lack of nutrients, prevent premature birth, prevent iatrogenic blood loss, such as frequent blood tests and unnecessary unnecessary laboratory tests.

Premature infant anemia complications Complications neonatal apnea

Severe cases can be apnea, growth disorders, nutritional deficiencies, and easy to concurrent infection.

Symptoms of anemia in premature infants Common symptoms After exercise, shortness of breath, tachycardia, edema, pale

Anemia symptoms

Pale, feeding difficulties, weight loss, shortness of breath, tachycardia, decreased activity, apnea, etc.

2. Edema

A few cases have lower extremities, feet, scrotum, and mild edema on the face.

Examination of anemia in premature infants

Blood routine

Generally positive cell positive pigment anemia, reticulocytes are normal or elevated.

2. Plasma erythropoietin

Normal 4 ~ 25U / L, premature infants reduced and not proportional to the degree of anemia.

3. Serum ferritin

Normal 194 ~ 238g / L 3 months ago, less than 10 ~ 20g / L, suggesting iron deficiency.

Routine chest X-ray examination, except for inflammatory changes in the lungs, ECG has a rapid increase in heart rhythm, B-ultrasound can be found in the liver and spleen.

Diagnosis and diagnosis of anemia in premature infants

diagnosis

Diagnosis can be confirmed based on clinical features and laboratory tests.

Differential diagnosis

First, except for infectious diseases and neonatal hemorrhagic disease, the differential diagnosis should be confirmed by physical examination and laboratory and auxiliary examination.

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