Kernicterus Medication

Updated: Dec 20, 2020
  • Author: Shelley C Springer, JD, MD, MSc, MBA, FAAP; Chief Editor: Ted Rosenkrantz, MD  more...
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Medication Summary

No medications are available to treat the symptoms of acute or chronic bilirubin encephalopathy. Pharmacologic intervention is aimed at prevention. Current therapies are indicated as adjuncts to phototherapy when total bilirubin is approaching exchange level; experimental therapy continues with the use of bilirubin production inhibitors.


Blood Product Derivatives

Class Summary

These methods decrease the amount of free bilirubin in the intravascular space, thus theoretically reducing the risk of neurotoxicity. Bilirubin is produced via induction of its enzymatic pathway and by RBC degradation. Inhibition of either of those 2 mechanisms can decrease the amount of bilirubin in the blood.

Albumin (Albuminar, Albutein, Plasbumin)

Because bilirubin bound to albumin is not available to cross the blood-brain barrier, increasing the amount of serum albumin theoretically increases the amount of available binding sites and decreases free bilirubin. Efforts to quantify albumin-binding capability or serum levels of bound bilirubin have not proved to be clinically useful, although assessment of the bilirubin-to-albumin ratio have been incorporated into the decision-making algorithm for exchange transfusion. However, administration of albumin for the purpose of increasing bilirubin-binding capacity is not a recommended standard of care. It may be considered in cases of significant hypoalbuminemia. Measured albumin levels < 3 g/dL may be considered an additional risk factor for BIND when considering therapeutic interventions.

Immune globulin intravenous (Gamimune, Gammagard S/D, Gammar-P, Polygam S/D)

Parenteral administration has been shown in controlled clinical trials to reduce the need for exchange transfusion in both Rh and ABO immune-mediated hemolytic disease. Its mechanism of action is not entirely clear.

Administration in hyperbilirubinemia resulting from isoimmune hemolytic disease that is unresponsive to phototherapy and/or is approaching exchange level has been recommended by the AAP in its 2004 revised clinical practice guideline.


Anticonvulsant Agents

Class Summary

Phenobarbital may increase hepatic conjugation and excretion. Decreased hepatic conjugation caused by normal delay in enzyme induction increases the amount of unconjugated bilirubin in the blood stream. Conjugated bilirubin does not pose a threat of neurotoxicity. Once conjugated, this nontoxic form of bilirubin proceeds toward intestinal excretion.

Phenobarbital (Luminal, Solfoton)

Induces the hepatic enzymes involved in bilirubin conjugation and increases biliary excretion.

Do not administer intra-arterially. Dosing can be enteral or parenteral.