Hemolytic disease of the newborn pathophysiology

Hemolytic disease of the newborn Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Hemolytic disease of the newborn from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Hemolytic disease of the newborn pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Hemolytic disease of the newborn pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Hemolytic disease of the newborn pathophysiology
CDC on Hemolytic disease of the newborn pathophysiology
Hemolytic disease of the newborn pathophysiology in the news
Blogs on Hemolytic disease of the newborn pathophysiology
Directions to Hospitals Treating Hemolytic disease of the newborn
Risk calculators and risk factors for Hemolytic disease of the newborn pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Antibodies are produced when the body is exposed to an antigen foreign to the make-up of the body. If a mother is exposed to an alien antigen and produces IgG (as opposed to IgM which does not cross the placenta), the IgG will target the antigen, if present in the fetus, and may affect it in utero and persist after delivery. The three most common models in which a woman becomes sensitized toward (i.e., produces IgG antibodies against) a particular blood type are:

• Fetal-maternal hemorrhage can occur due to trauma, abortion, childbirth, ruptures in the placenta during pregnancy, or medical procedures carried out during pregnancy that breach the uterine wall. In subsequent pregnancies, if there is a similar incompatibility in the fetus, these antibodies are then able to cross the placenta into the fetal bloodstream to attach to the red blood cells and cause hemolysis. In other words, if a mother has anti-RhD (D being the major Rhesus antigen) IgG antibodies as a result of previously carrying a RhD-positive fetus, this antibody will only affect a fetus with RhD-positive blood.

• The woman may receive a therapeutic blood transfusion with an incompatible blood type. ABO blood group system and Rhesus blood group system typing are routine prior to transfusion. Suggestions have been made that women of child bearing age or young girls should not be given a transfusion with Rhc-positive blood or Kell₁-positive blood to avoid possible sensitization, but this would strain the resources of blood transfusion services, and it is currently considered uneconomical to screen for these blood groups.

• The third sensitization model can occur in women of blood type O. The immune response to A and B antigens, that are widespread in the environment, usually leads to the production of IgM anti-A and IgM anti-B antibodies early in life. On rare occasions, IgG antibodies are produced. In contrast, Rhesus antibodies are generally not produced from exposure to environmental antigens.

Associated conditions

• Acquired hemolytic anemia
• Congenital toxoplasma
• Syphilis infection
• Congenital obstruction of the bile duct and cytomegalovirus infection.