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Obstetrics and Gynecology · Obstetrics

Prevention of rhesus incompatibility

Morbus haemolyticus neonatorum

Lack of adequate Rhesus conflict prevention leads to the development of hemolytic disease of the newborn (HDN). This severe condition arises due to the destruction of fetal erythrocytes, manifesting as anemia, jaundice, and varying degrees of edema syndrome.

Mild formManifests with pallor and a hemoglobin drop below 140 g/L; jaundice is minimal.
Common formAnemia with jaundice — accompanied by hepatosplenomegaly and hyperbilirubinemia.
KernicterusThreatens with seizures and the «setting-sun sign» in bilirubin encephalopathy.
Severe degreeCord blood hemoglobin drops below 100 g/L, and bilirubin exceeds 136.9 µmol/L.
5 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Clinical forms of hemolytic disease of the newborn

Ineffectiveness or absence of Rhesus conflict prevention leads to the manifestation of hemolytic disease of the newborn. In clinical practice, three main forms of this pathology are distinguished, differing in severity and prognosis.

  1. Hemolytic anemia without jaundice and hydrops. This is the mildest variant of the disease course. At birth, the main visual sign is pronounced pallor of the infant's skin. Laboratory diagnostics show a decrease in hemoglobin levels (Hb drops below 140 g/L). Jaundice syndrome in this form is either completely absent or appears only on the second or third day of life, while being extremely mild.
  1. Hemolytic anemia with jaundice. This is the most common variant of the pathology. Unlike physiological jaundice, which makes itself known on days 2–3, in this form, yellowish discoloration of the skin and visible mucous membranes is recorded at birth or shortly thereafter. Examination reveals enlargement of the liver (hepatomegaly) and spleen (splenomegaly). Laboratory tests show a decrease in hemoglobin against the background of hyperbilirubinemia. If the child remains untreated within the next 2–3 days, jaundice rapidly progresses, and the general condition worsens. Symptoms of bilirubin intoxication develop: the infant becomes lethargic, innate unconditional reflexes decrease, and dangerous episodes of apnea occur. With further progression, bilirubin encephalopathy (kernicterus) develops. Its characteristic signs are pronounced restlessness, increased extensor muscle tone, tonic seizures, and the specific «setting-sun sign».
  1. Hemolytic anemia with jaundice and hydrops. This is the most severe form of the disease, which very frequently ends in intrauterine fetal death or neonatal death. The clinical picture includes generalized edema, massive fluid accumulation in serous cavities (ascites, hydropericardium, hydrothorax develop), as well as a pronounced hemorrhagic syndrome. The liver and spleen are sharply enlarged and dense — this occurs due to the formation of extensive foci of extramedullary hematopoiesis within them. Laboratory tests confirm severe anemia and thrombocytopenia.

Criteria for hemolysis severity

The severity of the newborn's condition in Rhesus conflict is classified depending on the intensity of the erythrocyte destruction process. For an accurate and objective assessment, cord blood parameters are analyzed immediately after birth.

Clinical signMildModerate severitySevere
Anemia (Hb in cord blood)>150 g/L (>15 g%)149–100 g/L (15.1–10.0 g%)<100 g/L (<10 g%)
Jaundice (bilirubin in cord blood)<85.5 µmol/L (<5.0 mg%)85.6–136.8 µmol/L (5.1–8.0 mg%)>136.9 µmol/L (>8.0 mg%)
Edema syndromePuffiness of subcutaneous tissuePuffiness of subcutaneous tissueAscites or universal edema
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Principles of treatment for hemolytic disease

Therapeutic tactics directly depend on the clinical form and severity of the condition. In managing the mild form of HDN, the basis is careful monitoring: physicians are required to daily monitor the levels of hemoglobin, hematocrit, and bilirubin in the newborn's blood.

If strict indications arise, medical correction of anemia is performed. For this purpose, a transfusion of Rhesus-negative red blood cell suspension is administered, which must exactly match the newborn's blood group. The blood transfusion technique requires placing a catheter in a central or peripheral vein. Administration of the drug is carried out strictly using a syringe pump, while the infusion rate is maintained at 3–5 ml/h. During the transfusion procedure, medical staff continuously monitor blood pressure, heart rate, and diuresis.

The most important component of treatment is infusion therapy. Its main goals are detoxification of the body, increasing the bilirubin-binding capacity of serum blood albumin, and correction of concomitant metabolic disorders. A 10% dextrose (glucose) solution is used as the starting drug for intravenous infusions.

Briefly: answers to topical questions

Which specific prophylaxis drugs for Rhesus conflict are administered to pregnant women?

For the specific prevention of Rhesus conflict, anti-Rhesus immunoglobulin is administered to pregnant women.

  • Human anti-Rhesus immunoglobulin (Rho[D] or Rh0(D)) is a medication containing specific antibodies that bind to fetal antigens present in the mother's body, leading to the suppression of the immune response.

The drug is administered intramuscularly at a dose of 1250–1500 IU (250–300 mcg) for antenatal prophylaxis during pregnancy. After childbirth or pregnancy termination, a dose of 1500 IU (300 mcg) is used.

At what gestational ages is routine antenatal prophylaxis of Rhesus conflict performed?

Routine scheduled antenatal prophylaxis of Rhesus conflict is performed at 28–30 weeks of gestation. The prerequisite is the Rhesus-negative blood type of the mother and the absence of anti-Rhesus antibodies. If scheduled prophylaxis is missed, it is indicated after 28 weeks of gestation. Additional administration of immunoglobulin is prescribed to Rhesus-negative pregnant women with a negative level of anti-Rhesus antibodies during invasive procedures: amniocentesis, cordocentesis, chorionic villus sampling, or placentocentesis.

How to memorize

How to quickly memorize the three forms of hemolytic disease of the newborn (HDN) by severity: A (Anemia only) → A+J (Anemia + Jaundice) → A+J+E (Anemia + Jaundice + Edema/hydrops).

Class and exam questions

How to distinguish the icteric form of HDN from physiological jaundice?

In HDN, yellowish staining of the skin and mucous membranes appears at birth or shortly thereafter. Physiological jaundice occurs later — only on the 2nd–3rd day of life.

Why do the liver and spleen enlarge in severe HDN?

A sharp enlargement and induration of these organs (hepatosplenomegaly) occurs due to the formation of extensive foci of extramedullary hematopoiesis within them in response to massive hemolysis.

What type of blood is used to correct anemia in a newborn?

Rhesus-negative red blood cell suspension is used, which strictly matches the newborn's own blood group. The transfusion is performed slowly, at a rate of 3–5 ml/h.

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What else to study on this topic

  • Dynamics of bilirubin encephalopathy symptoms (apnea, decreased reflexes).
  • Full list of medications for HDN infusion therapy.
  • Mechanisms for increasing the bilirubin-binding capacity of albumin.
  • Technique for central venous catheter placement for blood transfusion.

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