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A Newborn Infant With Oxygen Desaturation During Sleep FREE TO VIEW

Ashley Deschamp, MD; Ameet Daftary, MD
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Division of Pediatric Pulmonology, Allergy and Sleep Medicine, Riley Hospital for Children at Indiana University Health, Indianapolis, IN

CORRESPONDENCE TO: Ashley Deschamp, MD, Division of Pediatric Pulmonology, Allergy and Sleep Medicine, Riley Hospital for Children at Indiana University Health, 705 Riley Hospital Dr, ROC 4270, Indianapolis, IN 46202-5225


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(1):e17-e20. doi:10.1016/j.chest.2016.08.1435
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The patient is a 1-week-old boy born at 37+2 weeks' gestational age through spontaneous vaginal delivery. The pregnancy was complicated by maternal gestational diabetes mellitus and pre-eclampsia. The Apgar score was 9 at both 1 minute and 5 minutes after birth. Because of hypoglycemia at delivery that required IV dextrose, he was admitted to the local neonatal intensive care unit. His blood glucose levels quickly stabilized, dextrose administration was discontinued, and the patient began breast-feeding. On day 2 of life, the patient began having intermittent oxygen desaturation, with oxygen saturation as measured by pulse oximetry down to 70% while sleeping; he was transferred to a tertiary-care NICU for further management. Aside from the hypoxia, he was otherwise asymptomatic. He was breast-feeding without difficulty and had no vomiting or gastroesophageal reflux; no cyanosis, stridor, or snoring; and no seizure-like activity or hypertonicity.

Figures in this Article

The patient's temperature was 36.8°C, heart rate was 114 beats per minute, blood pressure was 72/47 mm Hg, respiratory rate was 35 breaths/min, and oxygen saturation was 99% on room air with the patient awake. He was well nourished with no acute distress. His pupils were equal, round, and reactive to light. He was normocephalic, and the anterior fontanelle was open, soft, and flat. The lungs were clear to auscultation bilaterally, with no retractions or adventitious sounds. The heart had a regular rate and rhythm with no murmur. Normal peripheral perfusion was seen. There was normal muscle tone, strength, and range of motion throughout. The abdomen was soft and not tender or distended, and no organomegaly was present.

Head ultrasonography, echocardiography, and chest radiography results were all negative. A sepsis workup, including complete blood count, electrolyte panel, and blood culture, was negative. Six-hour polysomnography was performed to further evaluate the desaturation during sleep. Monitoring included electroencephalography, electromyography, electrocardiography, respiratory inductance plethysmography, thermistor, pressure transducer airflow readings, pulse oximetry, and end-tidal CO2 monitoring. The polysomnographic findings are shown in Figures 1 and 2.

Figure 1
Figure Jump LinkFigure 1 A 30-second epoch of non-rapid eye movement sleep showing characteristic trace alternans pattern in the electroencephalogram.Grahic Jump Location
Figure 2
Figure Jump LinkFigure 2 A 120-second epoch showing recurrent central apneas (periodic breathing) in non-rapid eye movement sleep.Grahic Jump Location

What is the diagnosis?

Diagnosis: Primary central sleep apnea of infancy

The infant had mixed sleep apnea with a predominance of periodic breathing (approximately 15% of total sleep time) and associated oxygen desaturation (desaturation index = 33/h). Figure 1 confirms the occurrence of events in non-rapid eye movement sleep as supported by the characteristic trace alternans pattern on the electroencephalogram. Figure 2 shows a prolonged run of central apnea (periodic breathing) in a 120-s polysomnographic epoch. The apnea hypopnea index (AHI) was 49 events/h, with improvement to six events per hour when the patient received 0.25 L/min oxygen through a nasal cannula. The American Academy of Sleep Medicine requires four criteria be met for this diagnosis: (1) gestational age ≥ 37 wk, (2) presence of central apnea, (3) recurrent prolonged central apnea (>20 s) or periodic breathing ≥ 5% of total sleep time on monitoring, and (4) findings that are not better explained by another disorder or medication. This entity must be distinguished from normal respiratory pauses, either isolated or after sigh, breaths, or movements. The patient in our study met these four diagnostic criteria.

Primary central sleep apnea of infancy is a well-recognized, though oftentimes forgotten entity in infancy. There is a predominance of central events; however, mixed and obstructive apnea may be present. Sleep apnea during infancy results from the interplay of three important mechanisms. First, in normal breathing, an increase in upper airway muscle tone is required prior to diaphragmatic contraction for unobstructed inspiration to occur. In newborn infants, this sequence of events may be altered, leading to upper airway collapse and airway obstruction during inspiration. Next, immaturity of respiratory control results in overcompensation for changes in CO2 and oxygen levels through a mechanism known as “loop gain,” which refers to the magnitude of ventilatory response for a given gas exchange disturbance. Those with high loop gain are prone to respiratory instability, whereas those with low loop gain are quite resistant to periodic breathing. Loop gain is affected by many components, including the central respiratory controller, the efficiency of CO2 excretion, and the delays imposed by hemoglobin binding and the circulation. Any of these various “gains” can serve to elevate the overall loop gain and create a propensity for breathing instability. Finally, a lower functional residual capacity in infants leaves less available oxygen stores. This, accompanied by a high loop gain, predisposes infants to respiratory instability.

The onset of primary central sleep apnea of infancy is usually in the first weeks to months of life. Workup may include investigation for infection, anemia, metabolic disturbances, medication effects, trauma, seizure, congenital central hypoventilation syndrome, and Chiari malformation. In cases of brief resolved unexplained events, primary central sleep apnea of infancy may be considered in the differential diagnosis. Although it is known that the frequency and prevalence of symptomatic apnea decreases with age, intervention may be necessary to ameliorate the risk for severe oxygen desaturation during apnea in infants with physiologically low functional residual capacity.

First, supplemental oxygen may be used to increase the oxygen reserve and decrease loop gain. However, even oxygen supplementation is not without adverse effects and can become ineffective with dislodgement or mucous plugging of the delivery interface. Also, a recent study in infant rats showed that hyperoxia leads to inflammation, with alveolar perturbation and leukocyte infiltration. CPAP may be used as well. An animal study showed that CPAP ameliorated recurrent central apnea by increasing lung volume and decreasing the cycle of loop gain, making it a potential option in more severe cases. Another option is to target the neurotransmitters involved in respiratory control. Methylxanthines, such as caffeine citrate, have been used in clinical practice to reduce apnea since the 1970s. The mechanism of action is uncertain, but possibilities include increased chemoreceptor responsiveness to CO2, enhanced respiratory muscle performance, and generalized central nervous system excitation.

Overall, the prognosis is good with resolution of findings over time. It is important to note that infant sleep apnea is not an established risk factor for sudden infant death syndrome. Also, persistent apnea may indicate an underlying medical condition requiring further workup.

Clinical Course

Treatment options considered at the time of diagnosis included supplemental oxygen vs caffeine citrate. Because of the ease of therapy, the family elected for caffeine therapy and he received an initial loading dose followed by maintenance therapy. A repeated polysomnogram after 48 h of enteral caffeine showed marked improvement in periodic breathing and central apnea, with the AHI improving to 14 events/h. He was discharged home on room air, caffeine citrate, and an apnea monitor. At 2 months of age, he was evaluated and was doing well with no apnea monitor alarms. He was weaned off caffeine. A repeated polysomnogram showed improvement of the AHI to 9.6 events/h with normal gas exchange, and the decision was made to follow him clinically. At 13 months of age, he again underwent polysomnography to assess for residual abnormalities. His AHI was 1.1 events/h without oxygenation or ventilation abnormalities, showing complete resolution of the patient’s primary central sleep apnea of infancy.

  • 1.

    Primary central sleep apnea of infancy occurs in term infants ≥ 37 weeks' gestation. Providers should consider this entity in cases of central apnea and brief resolved unexplained events, as treatment intervention may be necessary and effective.

  • 2.

    Pulse oximetry screening in newborn nurseries may be the first means of detection; however, polysomnography is diagnostic and typically demonstrates central apneas and periodic breathing.

  • 3.

    Caffeine citrate and oxygen can be effective therapies for primary central sleep apnea of infancy and often are only needed short-term until the infant’s control of breathing matures. The prognosis is generally good, as the condition resolves with age.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.


Figures

Figure Jump LinkFigure 1 A 30-second epoch of non-rapid eye movement sleep showing characteristic trace alternans pattern in the electroencephalogram.Grahic Jump Location
Figure Jump LinkFigure 2 A 120-second epoch showing recurrent central apneas (periodic breathing) in non-rapid eye movement sleep.Grahic Jump Location

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