ABO Hemolytic Disease of the Newborn

Etiology and clinical presentation

The development of an ABO immunological conflict is definitively diagnosed in the presence of blood group incompatibility. The most typical scenario: the mother has blood group 0(I) and is Rhesus-positive (Rh+), while her baby inherits blood group A(II) Rh+.

In clinical practice, a moderately severe icteric-edematous form is frequently observed. A full-term newborn (e.g., at 39 weeks of gestation) typically exhibits the following symptoms:

• Pronounced jaundice of the skin.
• Edema of soft tissues.
• General restlessness of the infant.
• Hepatosplenomegaly: enlargement of the liver (up to +2.5 cm below the costal margin) and spleen (up to +0.5 cm).

At the same time, severe anemia may be absent at the initial examination. Peripheral blood parameters may remain within normal limits: the hemoglobin level is around 170 g/L, and red blood cells are 4.3×10¹²/L.

Management tactics and monitoring

The basis for monitoring the condition of a newborn with HDN is emergency and thorough tracking of laboratory parameters. The physician's clinical reasoning is built on continuous assessment of free (unconjugated) bilirubin levels in the blood serum.

The key parameter is the hourly increase in unconjugated bilirubin. Decisions on treatment selection are based precisely on the dynamics of these figures: ranging from the initiation of intensive phototherapy to emergency surgical intervention upon reaching critical values.

Indications for surgical treatment

In the case of rapidly escalating intoxication, exchange transfusion (ETRT) is performed. This is a radical method that allows for the rapid removal of toxic bilirubin and antibodies from the bloodstream.

Strict indications for ETRT:

1. The hourly increase rate of unconjugated bilirubin exceeds 6–10 µmol/L.
2. The absolute value of unconjugated bilirubin in peripheral blood exceeds 340 µmol/L within the first 24 hours of the newborn's life.

Conservative therapy

If bilirubin levels remain below the critical thresholds for surgical intervention, as well as in the postoperative period, comprehensive conservative therapy is administered.

Main areas of treatment:

• Physiotherapy: phototherapy is the primary method for converting toxic unconjugated bilirubin into a safe water-soluble form.
• Detoxification and nutrition: intravenous infusions of protein solutions and dextrose (glucose).
• Metabolic liver support: administration of B vitamins (thiamine, pyridoxine), ascorbic acid, and cocarboxylase. This is necessary to improve hepatic metabolism.
• Enterosorption: use of diosmectite (Smecta). The drug binds bilirubin directly in the intestinal lumen, thereby preventing its reabsorption into the bloodstream and promoting excretion.

Complications, prognosis, and prevention

In the absence of timely and adequate treatment, ABO HDN carries severe risks. The main threats are the development of severe anemia and bilirubin encephalopathy (kernicterus), which leads to irreversible damage to the central nervous system by toxic unconjugated bilirubin.

The prognosis with early initiation of comprehensive therapy is favorable: a full recovery of the child is possible.

Regarding prevention, unlike Rhesus incompatibility where anti-Rhesus immunoglobulin is used, no specific prevention exists for ABO sensitization. Physicians have access only to non-specific measures, which consist of the most adequate and careful management of pregnancy and labor.

What else to study on this topic

• Pathogenesis of bilirubin encephalopathy (kernicterus)
• Technique and complications of exchange transfusion (ETRT)
• Evaluation of hemogram parameters in various forms of HDN
• Mechanism of enterohepatic circulation of bilirubin and the role of sorbents
• Differential diagnosis of the icteric-edematous form of HDN

Other topics in «Chapter 2. Neonatology»

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