Apnea of Prematurity Treatment & Management

  • Author: Dharmendra J Nimavat, MD, FAAP; Chief Editor: Ted Rosenkrantz, MD   more...
 
Updated: Feb 1, 2012
 

Medical Care

Goal of medical therapy

The principal goals of treating apnea of prematurity (AOP) are to address its cause and to provide appropriate medical management. For example, bacterial sepsis that causes apnea is treated with antibiotics and other supportive therapies, whereas seizures require anticonvulsants. The use of assisted ventilation to manage severe apnea, bradycardia, and O2 desaturation can be life saving, and assisted ventilation and O2 may be required to prevent injury to the CNS. The primary disease process must be identified and treated.

When all causes of apnea other than prematurity are excluded during the diagnostic work-up, apnea of prematurity is the presumptive etiology. Caregivers must decide which intervention is appropriate given the severity of the patient's apnea, bradycardia, and O2 desaturation. For example, an infant who has an inadequate response to tactile stimulation and O2 administration and who requires airway suctioning and bag-mask ventilation to recover suggests a serious problem.

A useful strategy is to have a protocol that defines escalating treatments for apnea of prematurity. Depending on the frequency and the severity of apnea, bradycardia, and O2 desaturation, common treatments include stimulation (usually tactile), methylxanthine, or assisted ventilation (eg, nasal continuous positive airway pressure [CPAP], mechanical ventilation).[103]

Pantalitschka et al compared 4 modes of nasal respiratory support for apnea of prematurity in very low birthweight infants: intermittent positive pressure ventilation (IPPV) via a conventional ventilator or a variable flow device and CPAP via a variable flow device or a constant flow underwater bubble system.[104] In their randomized controlled trial with a crossover design, episodes of bradycardia or desaturation occurred at a rate of 6.7 per hour with the conventional ventilator in IPPV mode and at a rate of 2.8 and 4.4 per hour with the variable flow device in CPAP and IPPV mode, respectively (P< 0.03 for both compared with IPPV/conventional ventilator). Pantalitschka et al concluded that a variable flow nasal CPAP may be more effective than a conventional ventilator in nasal IPPV mode for treating apnea of prematurity.

Stimulation

Tactile stimulation is usually sufficient to terminate an isolated apneic event caused by central apnea. Stimulation akin to that used during neonatal resuscitation (eg, a gentle tap to the sole of the foot or rubbing the back) is often enough to terminate a central apnea. However, other measures may be required to treat an obstructive event or an episode of airway obstruction followed by central apnea.

If the upper airway is obstructed, repositioning the patient's head and neck or gently elevating the infant's jaw may alleviate the occlusion.

Use of a high-flow nasal cannula may open the airway enough to reduce obstructive apnea. As an alternative, high-flow oxygenation through a nasal cannula may be an agonist for receptors in the airway. Nasal irritation due to the cannula may prevent central apnea by causing arousal. Additional research is needed to ascertain the usefulness of high-flow nasal cannulas for treating apnea of prematurity.

Administration of O2

Supplemental oxygenation or bag-mask ventilation is indicated in infants with signs of bradycardia or desaturation.

Medical treatment is indicated when apneic episodes number 6-10 or more per day; when the infant does not respond to tactile stimulation; or when an event requires O2 and/or bag-mask ventilation to terminate apnea, bradycardia, and/or desaturation.

Avoid hyperoxia, which may increase the risk of retinopathy of prematurity (ROP).

Use of CPAP

CPAP has been used to treat apnea in preterm neonates, and it is indicated when the infant continues to have apneic episodes despite achieving a therapeutic serum level of methylxanthine.

CPAP is delivered with nasal prongs, a nasal mask, or a face mask with 3-6 cm of water pressure.

CPAP effectively treats mixed and obstructive apnea, but it has little or no effect on central apnea. This limitation suggests that CPAP may reduce the frequency of apnea by means of several mechanisms, including stabilization of the partial pressure of O2 (PaO2) by increasing the functional residual capacity (FRC), by altering the influence of stretch receptors on respiratory timing, or by splinting the upper airway in an open position.

Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Dharmendra J Nimavat, MD, FAAP  Assistant Professor of Clinical Pediatrics, Department of Pediatrics, Division of Neonatology, Southern Illinois University School of Medicine

Dharmendra J Nimavat, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics and American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Coauthor(s)

Michael P Sherman, MD  Professor, Department of Child Health, University of Missouri-Columbia School of Medicine; Director, Fellowship Training Program in Neonatal-Perinatal Medicine, NICU, Columbia Regional Hospital; Professor Emeritus, Department of Pediatrics, University of California, Davis, School of Medicine

Michael P Sherman, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, European Society for Paediatric Research, Perinatal Research Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Rene L Santin, MD  Consulting Staff, Department of Pediatrics, Division of Neonatology, Primary Care Centers of Eastern Kentucky

Disclosure: Nothing to disclose.

Rachel Porat, MD  Director, Neonatal Apnea Monitoring Program, Assistant Director, Division of Neonatology, Albert Einstein Medical Center; Associate Professor, Department of Pediatrics, Thomas Jefferson University

Rachel Porat, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Steven M Donn, MD  Professor of Pediatrics, University of Michigan Medical School; Director, Division of Neonatal-Perinatal Medicine, Department of Pediatrics, CS Mott Children's Hospital, University of Michigan Health System

Steven M Donn, MD is a member of the following medical societies: American Pediatric Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Arun K Pramanik, MD, MBBS  Professor of Pediatrics, Director of Neonatal Fellowship, Louisiana State University Health Sciences Center

Arun K Pramanik, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, National Perinatal Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Carol L Wagner, MD  Professor of Pediatrics, Medical University of South Carolina

Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD  Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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Central apnea is defined as the cessation of both airflow and respiratory effort. ECG = electrocardiogram; HR = heart rate; THO = thoracic impedance; FLOW = air flow; ACT = ; SpO2 = peripheral oxygen saturation; STAGE = sleep stage.
Polysomnogram. Mixed apnea contains elements of both central and obstructive apnea. ECG = electrocardiogram; HR = heart rate (bpm); THO = thoracic movement; FLOW = flow the from nose and mouth; ACT = gross body movement; SpO2 = peripheral oxygen saturation (%); STAGE = sleep stage, where AT = active sleep.
Polysomnogram. Periodic breathing is defined as periods of regular respiration for as long as 20 seconds followed by apneic periods no longer than 10 seconds that occur at least 3 times in succession. ECG = electrocardiogram; HR = heart rate (bpm); THO = thoracic movement; FLOW = flow the from nose and mouth; ACT = gross body movement.
 
 
 
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