Chapter 31: Pregnancy and Neonatal Haematology

Pregnancy induces a massive increase in blood plasma volume that outweighs the rise in red cell mass, often resulting in a diluted haemoglobin concentration known as physiological anaemia. This period places substantial nutritional demands on the mother, particularly regarding iron and folate, where deficiencies can lead to maternal anaemia or fetal developmental issues like neural tube defects. Platelet levels naturally decline, but clinical attention is required if they fall significantly, as seen in gestational thrombocytopenia, hypertensive disorders like pre-eclampsia or HELLP syndrome, and immune thrombocytopenic purpura (ITP), where maternal antibodies can cross the placenta and affect the newborn. The state of pregnancy is inherently hypercoagulable due to increased clotting factors and suppressed fibrinolysis, increasing the risk of venous thromboembolism and disseminated intravascular coagulation (DIC). This necessitates careful management of anticoagulant therapy, often preferring low molecular weight heparin over warfarin to avoid developmental risks to the fetus. Moving to neonatal health, infants typically present with high haemoglobin and large red blood cells at birth, followed by a decline as they adapt to life outside the womb. Neonatal anaemia may stem from blood loss, infection, or immune-mediated destruction, while disorders like fetomaternal alloimmune thrombocytopenia present severe risks for internal bleeding. A critical focus is placed on Haemolytic Disease of the Newborn (HDN), primarily driven by Rh incompatibility where maternal anti-D antibodies attack fetal red cells. Modern medicine prevents this via prophylactic anti-D immunoglobulin administration, though ABO incompatibility remains a frequent but typically milder cause of jaundice and anaemia. Diagnostic tools such as the Kleihauer test and Doppler ultrasonography of fetal blood flow are essential for monitoring these risks. Finally, the neonatal coagulation system is characterized by immature levels of vitamin K-dependent clotting factors, necessitating a specialized understanding of normal ranges to manage potential thrombotic or haemorrhagic complications in the first months of life.