Infant respiratory distress syndrome
Infant respiratory distress syndrome | |
---|---|
Other names | Neonatal respiratory distress syndrome [1] |
Chest X-ray of a case of IRDS, with fine granular opacities, air bronchograms and bell-shaped thorax | |
Specialty | Pediatrics, obstetrics |
Infant respiratory distress syndrome (IRDS), also called respiratory distress syndrome of newborn, or increasingly surfactant deficiency disorder (SDD),
IRDS affects about 1% of newborns and is the leading cause of morbidity and mortality in
IRDS is distinct from pulmonary hypoplasia, another leading cause of neonatal death that involves respiratory distress.[citation needed]
The European Consensus Guidelines on the Management of Respiratory Distress Syndrome highlight new possibilities for early detection, and therefore treatment of IRDS.[8] The guidelines mention an easy to use rapid point-of-care predictive test that is now available[9] and how lung ultrasound, with appropriate training, expertise and equipment, may offer an alternative way of diagnosing IRDS early.[10]
Signs and symptoms
IRDS begins shortly after birth and is manifested by fast breathing (more than 60 breaths per minute), a fast heart rate, chest wall retractions (recession), expiratory grunting, nasal flaring, and blue discoloration of the skin during breathing efforts.[citation needed]
As the disease progresses, the baby may develop ventilatory failure (rising carbon dioxide concentrations in the blood) and prolonged cessations of breathing ("apnea"). Whether treated or not, the clinical course for the acute disease lasts about two to three days. During the first day, the child worsens and requires more support. During the second day, the baby may be remarkably stable on adequate support and resolution is noted during the third day, heralded by a prompt diuresis. Despite huge advances in care, IRDS remains the most common single cause of death in the first month of life in the developed world. Complications include metabolic disorders (acidosis, low blood sugar), patent ductus arteriosus, low blood pressure, chronic lung changes and bleeding in the brain. The syndrome is frequently complicated by prematurity and its additional effect on other organ functions.[11]
Related disorders
Acute respiratory distress syndrome (ARDS) has some similarities to IRDS. Transient tachypnea of the newborn presents with respiratory distress syndrome in the Term child.[12]
Histopathology
The characteristic histopathology seen in babies who die from RDS was the source of the name "hyaline membrane disease". Waxlike layers of hyaline membrane line the collapsed alveoli of the lung. In addition, the lungs show bleeding, overdistention of airways, and damage to the lining cells.[citation needed]
Pathophysiology
The lungs of infants with respiratory distress syndrome are developmentally deficient in a material called surfactant, which helps prevent the collapse of the terminal air spaces (the future site of alveolar development) throughout the normal cycle of inhalation and exhalation. This deficiency of surfactant is related to inhibition from the insulin that is produced in the newborn, especially those of diabetic mothers.[13]
Pulmonary surfactant is a complex system of
Microscopically, a pulmonary surfactant-deficient lung is characterized by collapsed air spaces alternating with hyperexpanded areas, vascular congestion, and, in time,
Traditional diagnostic approach
The diagnosis is made by the clinical picture and the chest X-ray, which demonstrates decreased lung volumes (bell-shaped chest), absence of the thymus (after about six hours), a small (0.5–1 mm), discrete, uniform infiltrate (sometimes described as a "ground glass" appearance or "diffuse airspace and interstitial opacities") that involves all lobes of the lung and air-bronchograms (i.e. the infiltrate will outline the larger airways passages, which remain air-filled). In severe cases, this becomes exaggerated until the cardiac borders become indiscernible (a 'white-out' appearance).[citation needed]
Point-of-care lung maturity test
To improve clinical outcomes very early treatment with surfactant is necessary.[14] However, only about half of infants with a gestational age (GA) below 30 weeks need surfactant treatment[15][16] and prophylactic surfactant treatment increases the combined mortality and incidence of Bronchopulmonary Dysplasia (BPD) contrary to selective rescue surfactant treatment.[17] Therefore, there is a need for a rapid diagnostic test to guide early targeted surfactant treatment.[18]
Professor Henrik Verder has worked with lung-maturity diagnostics on gastric aspirates obtained at birth for over 15 years. With the introduction of surfactant treatment for IRDS, Henrik Verder developed additional lung maturity tests based on gastric aspirates (GAS); for example, the microbubble stability test[19] and lamellar body counts (LBC)[20] as well as a large randomised trial using lamellar body counts to guide surfactant treatment.[21] However, a common problem with all these methods is dilution with foetal urine. Additionally, the methods are time‐consuming laboratory tests and are too slow to be used as a point‐of‐care test (POC) to guide surfactant treatment.
Professor Henrik Verder, in collaboration with chemometric scientist Agnar Hoskuldsson, developed a rapid point-of-care method for predicting IRDS by measuring the lecithin-sphingomyelin ratio (L/S) in gastric aspirate (GA).[9] The new method, which is based on mid‐red Fourier Transform Infrared spectroscopy (FTIR),[22] was shown to measure the L/S ratio at birth with a high sensitivity.[9] This rapid bedside test for surfactant components in gastric aspirate is also now available, and clinical trials of this new point-of-care test to determine surfactant need at birth are underway.[23][9]
Lung ultrasound
Lung ultrasound, with appropriate expertise, equipment and training, may offer another alternative way of diagnosing IRDS at an earlier stage, without apparently resulting in more infants overall being treated.[10]
Prevention
Giving the baby's mother
In pregnancies of longer than 30 weeks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid by
Epidemiology
Infant respiratory distress syndrome (IRDS) is the leading cause of death in premature infants.[26] Despite only 1% of all birth complications being attributed to respiratory distress syndrome, there is a significantly higher prevalence in prematurely born babies.[27] Incidence rates of IRDS in premature infants born at 30 weeks of gestational age (GA) are at 50%, and rise even higher to 93% for infants born prematurely at 28 weeks of gestational age or younger.[27] IRDS is diagnosed within hours of delivery and usually leads to morbidity and mortality in preterm infants. There are many risk factors that can potentially cause IRDS. The most common risks factors that can potentially cause IRDS include male gender, white race, late preterm delivery, maternal diabetes, perinatal hypoxia (exposure to low oxygen) and ischemia (decreased blood flow), and low birth weight.[28] Seventy percent of babies diagnosed with respiratory distress syndrome are born between 29 and 34 weeks of gestational age and are 55% more likely to be male.[27] A study conducted at the Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network studied premature infants born between 22 and 37 weeks and the outcomes leading to IRDS. This study was conducted from 2002 to 2008. The incidence rate of IRDS for 24 weeks was 98%, for 34 weeks the incidence is 5%, and for 37 weeks the incidence rate was less than 1%. The results demonstrate that the incidence of IRDS increases with decreasing age at birth.[29]
According to a study from the University of Miami's Department of Pediatrics and Division of Neonatology, from the time range of 2003 to 2014, respiratory distress syndrome prevalence jumped from 170 per 1000 preterm live births to 360 per 1000 preterm live births nationwide in the United States.[30] This study population's duration under hospital care averaged 32 days in 2003, increasing by nearly a week to 38 days in 2014.[30] Additionally, this study yielded average prevalence rates of 260 cases per 1000 livebirths from the years of 2003 to 2014,[30] which coincided with the results yielded by a report from the Vermont Oxford Network in 2008 of 300 per 1000 livebirths.[31]
Treatment
Oxygen is given with a small amount of
INSURE (Intubation Surfactant Extubation) and LISA (Less Invasive Surfactant Administration) methods
The INSURE method has been shown, through meta-analysis, to successfully decrease the use of mechanical ventilation and lower the incidence of bronchopulmonary dysplasia (BPD).[36] Since its conception in 1989, the INSURE method has been academically cited in more than 500 papers.[37] The first randomised study involving the INSURE method was published in 1994[38] and a second randomised study in infants less than 30 weeks gestation was published by the group in 1999.[39] Based on the INSURE method, Henrik Verder has since developed a rapid bedside test that predicts IRDS at birth.[8]
Extracorporeal membrane oxygenation (ECMO)
Culture and society
- In 1963, Jacqueline Kennedy, died of RDS two days after his premature birth at 34 weeks gestation.[41]
- Two daughters of Dominick Dunne and his wife Ellen Griffin Dunne died of RDS, one in 1958 and one in 1963.[42]
See also
- Bubble CPAP
- Bronchopulmonary dysplasia
- Pulmonary hypoplasia
- Surfactant metabolism dysfunction
- Surfactant therapy
- Wilson–Mikity syndrome
References
- ^ "neonatal respiratory distress syndrome" at Dorland's Medical Dictionary
- PMID 5334613.
- PMID 23976885.
- ISBN 9780470670408; Access provided by the University of Pittsburgh)
{{cite book}}
: CS1 maint: postscript (link - ISBN 978-0-323-00929-4.
- PMID 23347658.
- ^ "Infant Respiratory Distress Syndrome. IRDS information". April 2022.
- ^ PMID 36863329.
- ^ PMID 31038796.
- ^ PMID 34320032.
- PMID 25274969.
- ^ "Acute Respiratory Distress Syndrome". The Lecturio Medical Concept Library. Retrieved 27 June 2021.
- PMID 3549256.
- PMID 23152207.
- S2CID 19431025.
- S2CID 38291029.
- ^ "Google Scholar". scholar.google.com. Retrieved 2023-05-23.
- PMC 6516810.
- PMID 12856986.
- S2CID 24024355.
- S2CID 2699650.
- PMID 27886403.
- PMID 36863329.
- ^ Men-Jean Lee; Debra Guinn; Charles J Lockwood; Vanessa A Barss. "Antenatal use of glucocorticoids in women at risk for preterm delivery". Retrieved December 16, 2013.
- PMID 24126948.)
{{cite journal}}
: CS1 maint: numeric names: authors list (link - PMID 30675087.
- ^ PMID 20732945.
- S2CID 102349516.
- PMID 22641761.
- ^ S2CID 58665454.
- PMID 20363446.
- ^ PMID 33058208.
- PMID 8164699.
- PMID 11809911.
- ^ Henrik, Verder (23 May 2023). "Research Gate".
- PMID 15266470.
- ^ "Henrik Verder research profile". www.Researchgate.net. Retrieved 15 July 2014.
- PMID 8090164.
- PMID 9925870.
- .
- ^ Altman, Lawrence (2013-07-29). "A Kennedy Baby's Life and Death". The New York Times. The New York Times. Retrieved 6 June 2015.
- ^ Dunne, Dominick (2008-04-08). "Justice". Vanity Fair. Retrieved 31 October 2019.