ABSTRACT
BACKGROUND:
Apnea of prematurity consists in 15 to 20 sec. of breathing cessation and is the most important disorder in the control of breathing in preterm infants. It is treated with caffeine citrate.
OBJECTIVES:
The objectives of this article are to review: (1) the mechanisms of action, (2) the effects, (3) the metabolism, (4) the pharmacokinetics, and (5) the adverse effects of caffeine citrate in preterms.
METHODS:
The bibliographic search was performed using PubMed and EMBASE databases as search engines and April 2014 was the cutoff point.
RESULTS:
Caffeine citrate is a stimulant of the respiratory and central nervous systems. It binds competitively to the receptors for adenosine A1 and A2A, causing inhibition. Caffeine increases respiratory rate and minute volume, stimulates respiratory centers, and increases pulmonary blood flow and the sensitivity of central medullary areas to hypercapnia. Orally administered caffeine citrate is rapidly and completely absorbed. It is N-demethylated by CYP1A2 and is N-acetylated by N-acetyltransferase. The half-life of caffeine citrate is 100 hours at birth and 5 hours at a gestational age >29 weeks. There is a remarkable shortening of the half-life during neonatal maturation. Adverse effects of caffeine are usually mild, and include restlessness, vomiting, and functional cardiac symptoms.
CONCLUSIONS:
Caffeine citrate is the drug of choice for the treatment of apnea of prematurity. It is an easy drug to use. Administered orally or intravenously once a day, it does not require monitoring of serum concentrations and has few side effects.
KEYWORDS:
caffeine citrate; metabolism; neonate; pharmacodynamics; pharmacokinetics