Prenatal Blood Loss

Transplacental Fetomaternal

In 50% of pregnancies, fetal cells can be demonstrated in the maternal circulation, and in 1% of cases this is of sufficient magnitude to produce anemia in the infant. Transplacental blood loss may be acute or chronic. Table 2-2 lists the characteristics of acute and chronic blood loss in the newborn. Blood loss may be secondary to procedures such as diagnostic amniocentesis or external cephalic version. Fetomaternal hemorrhage is diagnosed by demonstrating fetal red cells by the acid-elution method of staining for fetal hemoglobin (Kleihauer-Betke technique) in the maternal circulation. The optimal timing for demonstrating fetal cells in maternal blood is within 2 hours of delivery and no later than the first 24 hours following delivery.

Intraplacental and Retroplacental

Occasionally, fetal blood accumulates in the substance of the placenta (intraplacental) or retroplacentally, and the infant is born anemic. Intraplacental blood loss from the fetus may occur when there is a tight umbilical cord around the neck or body or when there is delayed cord clamping. Retroplacental bleeding from abruptio placenta is diagnosed by ultrasound or at surgery.

Anemia During the Neonatal Period 13 Table 2-1. Causes of Anemia in the Newborn

I. Hemorrhage

A. Prenatal

1. Transplacental fetomaternal (spontaneous, traumatic amniocentesis, external cephalic version)

2. Intraplacental

3. Retroplacental

4. Twin-to-twin transfusion

B. Intranatal

1. Umbilical cord abnormalities a. Rupture of normal cord (unattended labor)

b. Rupture of varix or aneurysm of cord c. Hematomas of cord d. Rupture of anomalous aberrant vessels of cord (not protected by Wharton's jelly)

e. Vasa previa (umbilical cord is presenting part)

f. Inadequate cord tying

2. Placental abnormalities a. Multilobular placenta (fragile communicating veins to main placenta)

b. Placenta previa—fetal blood loss predominantly c. Abruptio placentae—maternal blood loss predominantly d. Accidental incision of placenta during cesarean section

C. Postnatal

1. External a. Bleeding from umbilicus b. Bleeding from gut c. Iatrogenic (diagnostic venipuncture, post-exchange transfusion)

2. Internal a. Cephalhematomata b. Subaponeurotic hemorrhage c. Subdural or subarachnoid hemorrhage d. Intracerebral hemorrhage e. Intraventricular hemorrhage f. Retroperitoneal hemorrhage (may involve adrenals)

g. Subcapsular hematoma or rupture of liver h. Ruptured spleen

II. Hemolytic anemia (see Chapter 7) A. Congenital erythrocyte defects

1. Membrane defects (with characteristic morphology)

a. Hereditary spherocytosis (pages 143-147)

b. Hereditary elliptocytosis (pages 147-148)

c. Hereditary propoikilocytosis (pages 148-149)

d. Hereditary stomatocytosis (pages 149-150)

e. Hereditary acanthocytosis (page 150)

f. Hereditary xerocytosis (pages 150-151)

g. Infantile pyknocytosisa

2. Hemoglobin defects a. a-Thalassemia6

b. y ß-Thalassemia c. Unstable hemoglobins (Hb Köln, Hb Zürich6) (pages 180-181)

3. Enzyme defects a. Embden-Meyerhof glycolytic pathway

(1) Pyruvate kinase

(2) Other enzymes b. Hexose-monophosphate shunt

(1) G6PD (Caucasian and Oriental) with or without drug exposure6

(2) Enzymes concerned with glutathione reduction or synthesis6

Table 2-1. (Continued)

B. Acquired erythrocyte defects

1. Immune a. Rh disease, ABO, minor blood groups (M, S, Kell, Duffy, Luther)

2. Nonimmune a. Infections (cytomegalovirus, toxoplasmosis, herpes simplex, rubella, syphilis, bacterial sepsis, e.g., Escherichia coli)

b. Microangiopathic hemolytic anemia with or without disseminated intravascular coagulation: disseminated herpes simplex, coxsackie B infections, gram-negative septicemia, renal vein thrombosis c. Toxic exposure (drugs, chemicals) ± G6PD ± prematurity6: synthetic vitamin K analogues, maternal thiazide diuretics, antimalarial agents, sulfonamides, naphthalene, aniline-dye marking ink, penicillin d. Vitamin E deficiency e. Metabolic disease (galactosemia, osteopetrosis)

III. Failure of red cell production

1. Congenital (Chapter 6) Diamond-Blackfan anemia (pure red cell aplasia) Dyskeratosis Congenita

Fanconi anemia

Congenital dyserythropoietic anemia

2. Acquired

Viral infection (hepatitis, HIV, CMV, rubella, syphilis, parvovirus) Anemia of prematurity

"Not permanent membrane defect but has characteristic morphology.

11 All of these conditions can be associated with Heinz-body formation and in the past were grouped together as congenital Heinz-body anemia.

Table 2-2. Characteristics of Acute and Chronic Blood Loss in the Newborn


Acute blood loss

Chronic blood loss


Acute distress; pallor; shallow,

Marked pallor disproportionate

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