Overview
Introduction
In the fetus, severe hemolysis causes anemia. Anemia reduces oxygen carrying capacity, so the fetal heart compensates by pumping faster and harder.
In the fetus, severe hemolysis causes anemia. Anemia reduces oxygen-carrying capacity, so the fetal heart compensates by pumping faster and harder. If compensation fails, the fetus may develop hydrops fetalis, which means abnormal fluid accumulation in fetal tissues or body cavities. In the newborn, the most visible sign is jaundice, especially jaundice that appears early, progresses rapidly, or is associated with poor feeding, lethargy, hypotonia, high-pitched cry, or abnormal neurologic signs. Jaundice occurs because hemolysis produces bilirubin faster than the newborn liver can conjugate and eliminate it. Pallor occurs because red blood cells are being destroyed. Tachycardia, tachypnea, weak feeding, poor perfusion, low activity, temperature instability, and hypotension can occur when anemia becomes clinically significant. Hepatosplenomegaly may occur because the liver and spleen are involved in red blood cell destruction and compensatory blood cell production. Clinical trajectory check Link new findings to the underlying process and the compensatory response that is succeeding or failing. Reassess objective trends such as perfusion, oxygenation, mental status, pain pattern, labs, and response to time-limited interventions so the next action reflects improvement or deterioration rather...