Neonatal apnea, bradycardia, or desaturation: Does it matter?

doi:10.1016/S0022-3476(98)70297-5

The Journal of Pediatrics

Volume 132, Issue 5, May 1998, Pages 758-759

https://doi.org/10.1016/S0022-3476(98)70297-5 Get rights and content

Abstract

J Pediatr 1998;132:758-9

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Cited by (27)

A novel sleep oximetry scoring tool for pediatric laryngomalacia
2022, International Journal of Pediatric Otorhinolaryngology
Citation Excerpt :
As desaturations transition from tachycardia to bradycardia, with the HR reflecting the autonomic nervous system response, we selectively focused on bradycardic desaturations to capture physiologically significant obstructive events [14,15]. Existing literature has demonstrated the ominous importance of the decreased heart rate in signaling severe hypoxic events [16,17]. Additionally, incorporation of the HR metric in association with desaturations creates a higher threshold for abnormal findings, which is pertinent due to the wide breadth of presentation on the sleep oximetry.
Despite being a more accessible and less resource intensive modality than polysomnography, the utility of sleep oximetry (SO) in pediatric laryngomalacia (LM) is not well understood or validated. We aimed to retrospectively evaluate the utility of overnight home based SO in children with LM by developing and internally validating the Modified Laryngomalacia Oximetry Score (MLOS) scoring system to triage severity and guide clinical decision making.
We evaluated pediatric patients with a diagnosis of LM at our tertiary referral centre. Data from initial and post-treatment SO including mean oxygen saturation (spO2) nadir and mean oxygen desaturation index (ODI) were aggregated. The MLOS ranging from I-VI (inconclusive to severe) was created by two otolaryngologists to incorporate bradycardia associated desaturation events during SO. Corresponding McGill Oximetry Score (MOS) was also determined.
172 patients were included in final analysis. The average age was 9.2 ± 14.3 months. 98 (57%) of patients were identified as Thompson severity score 1, and 87 (50.6%) of patients underwent supraglottoplasty. The surgical cohort had a significantly higher MLOS and MOS scores of 4 and 2 respectively, and higher mean ODI and spO2 nadir metrics. When evaluating post-supraglottoplasty SO tracings, all parameters improved significantly, including median MLOS score from 4 to 1. Only the mean ODI improved in the non-surgical cohort. Patients with Thompson severity score 2/3 had significantly higher MLOS.
We present a simple scoring system based on overnight SO, the MLOS, to help triage severity of pediatric LM and guide decision-making. MLOS is associated with worse clinical severity and a need for surgery, and shows significant improvement after surgery.
Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity
2020, Respiratory Physiology and Neurobiology
Citation Excerpt :
Severe inflammation gives rise to sepsis and is the major cause of morbidity and mortality in neonatal populations (Fleischmann-Struzek et al., 2018). Sepsis also increases the incidence of mixed apneas (an obstructive apnea followed by central apnea) in preterm infants (Fanaroff et al., 1998; Martin and Fanaroff, 1998; Olsson et al., 2003; Hofstetter et al., 2008 and reviewed in Herlenius, 2011). One proposed mechanism for these respiratory impairments was investigated using sepsis-level LPS (100 mg/kg, i.p.).
The respiratory control network in the central nervous system undergoes critical developmental events early in life to ensure adequate breathing at birth. There are at least three “critical windows” in development of respiratory control networks: 1) in utero, 2) newborn (postnatal day 0-4 in rodents), and 3) neonatal (P10-13 in rodents, 2-4 months in humans). During these critical windows, developmental processes required for normal maturation of the respiratory control network occur, thereby increasing vulnerability of the network to insults, such as inflammation. Early life inflammation (induced by LPS, chronic intermittent hypoxia, sustained hypoxia, or neonatal maternal separation) acutely impairs respiratory rhythm generation, chemoreception and increases neonatal risk of mortality. These early life impairments are also greater in young males, suggesting sex-specific impairments in respiratory control. Further, neonatal inflammation has a lasting impact on respiratory control by impairing adult respiratory plasticity. This review focuses on how inflammation alters respiratory rhythm generation, chemoreception and plasticity during each of the three critical windows. We also highlight the need for additional mechanistic studies and increased investigation into how glia (such as microglia and astrocytes) play a role in impaired respiratory control after inflammation. Understanding how inflammation during critical windows of development disrupt respiratory control networks is essential for developing better treatments for vulnerable neonates and preventing adult ventilatory control disorders.
Low oxygen saturation target range is associated with increased incidence of intermittent hypoxemia
2012, Journal of Pediatrics
Citation Excerpt :
The effect of the duration of recovery time between intermittent hypoxemia events on the resultant oxidative stress response has yet to be determined and merits further investigation. Data are limited on the long-term consequences of intermittent hypoxemia events in preterm infants.18 Apnea of prematurity during hospitalization19 and cardiorespiratory events in the home20 have been associated with neurodevelopmental impairment, with only 1 study showing mean O2 saturation during apnea as a predictor of motor scores.21
To test the hypothesis that preterm infants randomized to a low vs high O₂ saturation target range have a higher incidence of intermittent hypoxemia.
A subcohort of 115 preterm infants with high resolution pulse oximetry enrolled in the Surfactant, Positive Pressure, and Oxygenation Randomized Trial were randomized to low (85%-89%) or high (91%-95%) O₂ saturation target ranges. Oxygen saturation was monitored until 36 weeks postmenstrual age or until the infant was breathing room air without respiratory support for ≥72 hours.
The low target O₂ saturation group had a higher rate of intermittent hypoxemia (≤80% for ≥10 seconds and ≤3 minutes) prior to 12 days and beyond 57 days of life (P < .05). The duration shortened (P < .0001) and the severity increased (P < .0001) with increasing postnatal age with no differences between target saturation groups. The higher rate of intermittent hypoxemia events in the low target group was associated with a time interval between events of <1 minute.
A low O₂ saturation target was associated with an increased rate of intermittent hypoxemia events that was dependent on postnatal age. The duration and severity of events was comparable between target groups. Further investigation is needed to assess the role of intermittent hypoxemia and their timing on neonatal morbidity.
An inflammatory pathway to apnea and autonomic dysregulation
2011, Respiratory Physiology and Neurobiology
Citation Excerpt :
Preterm infants have periodic unstable breathing that is sensitive to the environment (Barrington and Finer, 1991). A decreased respiratory drive and impaired pulmonary function predispose the premature infant to apnea and hypoventilation that in turn may precipitate desaturation and/or bradycardia (Martin and Fanaroff, 1998). Peripheral chemoreceptors are only active at very low oxygen levels during fetal life and become essentially silent in the immediate postnatal period due to the sudden increase in PO2 from <30 mm Hg to 50 to 70 mm Hg range or higher (Mathew, 2010).
Infection in infancy may dramatically aggravate an underlying cardiorespiratory dysfunction during a susceptible postnatal period. Children with immature brainstem respiratory control, as well as infants, may have periodic irregular breathing with potential detrimental apneas that are increased during sleep as well as during infectious episodes.
Data now indicate that the proinflammatory cytokine interleukin (IL)-1β impairs respiration during infection via prostaglandin E2 (PGE₂) and that infection, with associated eicosanoid release, is one of the main causes of respiratory disorders in preterm infants. Moreover, brainstem microsomal prostaglandin E synthase-1 (mPGES-1) is rapidly activated during transient hypoxia. An inflammatory mediated activation of the mPGES-1 pathway, e.g., by viral or bacterial infection, rapidly induces release of PGE₂ in the vicinity of brainstem cardio-respiratory-related centers. This will depress the autonomic control networks, including the central drive to breathe. Hypoxia may then further reduce the activity of vital brainstem centers and the ability to autoresuscitate. This might have fatal consequences in vulnerable infants during a susceptible time frame.
Here the evidence from human, animal and molecular studies to support this hypothesis is reviewed and how the pathogenesis of apnea and the response to hypoxia is associated with inflammatory pathways is discussed.
Laryngeal oedema in neonatal apnoea and bradycardia syndrome (a pilot study)
2005, Early Human Development
Some preterm infants in general good health continue to present recurrent apnoeas, bradycardias and desaturations (ABD) despite usual treatments. These events may lead to transitory brain hypoxia and to further neurological injury.
The purpose of this study has been to evaluate the role of laryngeal oedema in this symptomatology and to assess corticoid treatment.
Twelve preterm babies born at a median age of 28.5 weeks (range: 26–35 weeks) already showed signs of ABD at a median age of life of 28.5 days (range: 9–80 days). Fiberoptic laryngeal endoscopy was performed on these babies at a median postconceptional age of 34 weeks (range: 31–38 weeks) to detect a possible involvement of the larynx in their ABD.
Each patient presented a severe laryngeal oedema compatible with potential obstructive breathing. Half of the cohort (n=6) received inhaled corticosteroids initiated with a short oral dexamethasone treatment for 3 to 5 days (group 1). All the babies improved. The other half (n=6) received only an inhaled topic corticosteroid treatment (group 2). Four of the six babies improved and two needed oral dexamethasone. Laryngoscopic endoscopy was carried out after 1 week of treatment. The picture corresponded with clinical improvement. Recurrence of ABD occurred in 3/12 (25%) of the babies after stopping dexamethasone. No immediate side effects of the procedure or the treatment were observed.
Laryngeal oedema may be a cause of ABD in preterm newborns. It may arise from oesophageal reflux and/or presence of the feeding tube. It can be diagnosed by atraumatic fiberoptic fibroscopy and successfully treated with corticosteroids.
Control of Breathing
2005, Avery's Diseases of the Newborn

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Neonatal apnea, bradycardia, or desaturation: Does it matter?☆

Abstract

Respir Physiol

Respir Physiol

Respir Physiol

J Pediatr

J Pediatr

J Pediatr