Newborn Babies Who Cannot Maintain Proper Levels of Surfactant Die of:

Newborn Respiratory Distress

CHRISTIAN L. HERMANSEN, MD, MBA, and ANAND MAHAJAN, MD, Lancaster General Hospital, Lancaster, Pennsylvania

Am Fam Physician. 2015 Dec ane;92(xi):994-1002.

This clinical content conforms to AAFP criteria for continuing medical didactics (CME). See the CME Quiz Questions.

Author disclosure: No relevant financial affiliations.

• Abstruse
• Clinical Presentation
• Diagnosis
• Full general Treatment Principles
• Etiologies
• References

Article Sections

• Abstract
• Clinical Presentation
• Diagnosis
• Full general Handling Principles
• Etiologies
• References

Newborn respiratory distress presents a diagnostic and management challenge. Newborns with respiratory distress commonly exhibit tachypnea with a respiratory charge per unit of more than than threescore respirations per minute. They may present with grunting, retractions, nasal flaring, and cyanosis. Common causes include transient tachypnea of the newborn, respiratory distress syndrome, meconium aspiration syndrome, pneumonia, sepsis, pneumothorax, persistent pulmonary hypertension of the newborn, and delayed transition. Built centre defects, airway malformations, and inborn errors of metabolism are less common etiologies. Clinicians should be familiar with updated neonatal resuscitation guidelines. Initial evaluation includes a detailed history and physical examination. The clinician should monitor vital signs and measure oxygen saturation with pulse oximetry, and claret gas measurement may be considered. Chest radiography is helpful in the diagnosis. Claret cultures, serial complete claret counts, and C-reactive protein measurement are useful for the evaluation of sepsis. Most neonates with respiratory distress tin be treated with respiratory support and noninvasive methods. Oxygen tin can be provided via purse/mask, nasal cannula, oxygen hood, and nasal continuous positive airway pressure. Ventilator back up may exist used in more severe cases. Surfactant is increasingly used for respiratory distress syndrome. Using the INSURE technique, the newborn is intubated, given surfactant, and quickly extubated to nasal continuous positive airway pressure. Newborns should be screened for critical congenital centre defects via pulse oximetry subsequently 24 hours but earlier hospital belch. Neonatology consultation is recommended if the illness exceeds the clinician's expertise and comfort level or when the diagnosis is unclear in a critically ill newborn.

Newborn respiratory distress occurs in about 7% of deliveries.1 Respiratory distress syndrome, which occurs primarily in premature infants, affects nigh 1% of newborns, resulting in about 860 deaths per twelvemonth.two With increased survival of preterm and late preterm infants, management of respiratory distress in newborns has go challenging.3,4 Because early on recognition improves the care of these newborns, clinicians must exist familiar with its diagnosis and treatment.

SORT: Primal RECOMMENDATIONS FOR Do

Clinical recommendation	Bear witness rating	References	Comments
Noninvasive ventilation, unremarkably using nasal continuous positive airway pressure, may supersede invasive intubation because of improved clinical and financial outcomes.	B	15	Randomized controlled trial
The minimum required amount of surfactant is 100 mg per kg. Initial assistants of 200 mg per kg can upshot in significant improvement in oxygenation and decreased need to retreat.	B	17, 18	Randomized controlled trials
The INSURE (intubate, administer surfactant, extubate to nasal continuous positive airway force per unit area) strategy should be used to reduce mechanical ventilation, air leak syndromes, and progression to bronchopulmonary dysplasia.	B	19	Cochrane review
Antenatal corticosteroids given between 24 and 34 weeks' gestation decrease respiratory distress syndrome risk with a number needed to care for of 11.	C	vi	Consensus guidelines
The U.S. Department of Health and Human Services recommends screening newborns for critical congenital centre defects using pulse oximetry before infirmary discharge, but at least 24 hours after nativity.	C	53	Prospective written report

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WHAT IS NEW ON THIS TOPIC: NEWBORN RESPIRATORY DISTRESS

The U.Due south. Department of Health and Human Services recommends routine pulse oximetry over physical test solitary as a screening strategy for critical congenital heart disease.

Maternal selective serotonin reuptake inhibitor use late in pregnancy is associated with a modest absolute increased risk for persistent pulmonary hypertension of the newborn.

Reduction of premature births and cesarean deliveries decreases respiratory distress cases, with prenatal care being crucial to prevention. Women with inadequate prenatal care may evangelize babies with lower birth weights and increased risk of admission to the neonatal intensive care unit.v Antenatal corticosteroid use in threatened preterm deliveries from 24 to 34 weeks' gestation significantly reduces the incidence and severity of respiratory distress.6 Considering cesarean commitment is a chance factor for respiratory distress, especially in premature infants, reducing these surgeries when possible could reduce the incidence of the status.7

Clinical Presentation

• Abstract
• Clinical Presentation
• Diagnosis
• Full general Treatment Principles
• Etiologies
• References

Tachypnea is the most common presentation in newborns with respiratory distress. A normal respiratory rate is twoscore to lx respirations per minute. Other signs may include nasal flaring, grunting, intercostal or subcostal retractions, and cyanosis. The newborn may also have languor, poor feeding, hypothermia, and hypoglycemia.

The most mutual causes of respiratory distress in newborns are transient tachypnea of the newborn (TTN), respiratory distress syndrome (RDS), meconium aspiration syndrome, pneumonia, sepsis, pneumothorax, and delayed transition. Rare causes include choanal atresia; diaphragmatic hernia; tracheoesophageal fistula; built heart illness; and neurologic, metabolic, and hematologic disorders. The differential diagnosis of newborn respiratory distress is listed in Table ane.8

Table one.

Differential Diagnosis of Newborn Respiratory Distress

Pulmonary

Transient tachypnea of the newborn

Respiratory distress syndrome

Meconium aspiration

Pneumothorax

Persistent pulmonary hypertension of the newborn

Pulmonary hypoplasia

Tracheoesophageal fistula

Diaphragmatic hernia

Infectious

Pneumonia

Sepsis

Meningitis

Other

Delayed transition

Congenital heart disease

Hypoglycemia

Polycythemia or anemia

Choanal atresia

Hydrocephalus

Intracranial hemorrhage

Respiratory rate suppression from maternal narcotic apply

Inborn errors of metabolism

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Rarely, newborns with RDS develop chronic lung affliction or bronchopulmonary dysplasia. Definitions have been established for bronchopulmonary dysplasia severity (Table 2).nine Newborns with bronchopulmonary dysplasia may accept nutritional failure, take neurodevelopmental delays, and require oxygen for a longer period with higher infirmary readmission rates.10

Tabular array 2.

Diagnostic Criteria for Bronchopulmonary Dysplasia

Severity	Criteria
	Newborns born at < 32 weeks' gestation	Newborns born at ≥ 32 weeks' gestation
	Treatment with > 21% oxygen for at to the lowest degree 28 days plus:
Mild	Breathing room air at 36 weeks postmenstrual age or at discharge, whichever comes first	Breathing room air by 56 days postnatal age or discharge, whichever comes first
Moderate	Requires < xxx% oxygen at 36 weeks postmenstrual age or at discharge, whichever comes offset	Requires < 30% oxygen at 56 days postnatal age or at belch, whichever comes get-go
Astringent	Requires ≥ xxx% oxygen and/or positive pressure level (PPV or N-CPAP) at 36 weeks postmenstrual historic period or at discharge, whichever comes first	Requires ≥ thirty% oxygen and/or positive pressure (PPV or N-CPAP) at 56 days postnatal age or at belch, whichever comes get-go

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Diagnosis

• Abstract
• Clinical Presentation
• Diagnosis
• General Treatment Principles
• Etiologies
• References

A conscientious history and physical examination are imperative in the evaluation of newborns with respiratory distress. Additional workup options are included in Table iii.viii

Table 3.

Workup Options for Newborn Respiratory Distress

Test	Comments
Blood culture	May somewhen diagnose bacteremia Results are not considered negative until incubating for 48 hours
Blood gas	Assesses the degree of hypoxemia and acrid-base of operations condition
Blood glucose	Hypoglycemia can cause or beal tachypnea
Chest radiography	Differentiates various types of respiratory distress
Complete claret count with differential	Leukocytosis or left shift: stress or infection Neutropenia: bacterial infection Depression hemoglobin level: anemia High hemoglobin level: polycythemia Depression platelet count: sepsis Calculation of immature to total neutrophil ratio
C-reactive protein	Has a negative predictive value in assessing for infection
Pulse oximetry	Detects hypoxia and assesses the degree of oxygen requirement

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Laboratory data tin can assist in the diagnosis. Complete claret counts with an young to full neutrophil ratio of more than 0.2 is suggestive of infection. This ratio can be contradistinct by stress, crying, and labor induced with oxytocin (Pitocin).eleven Although the young to total neutrophil ratio has pregnant sensitivity and negative predictive value, information technology has poor positive predictive accuracy as a one-fourth dimension test and is falsely elevated in l% of infants without an infection.eleven C-reactive poly peptide levels of less than 10 mg per 50 (95.24 nmol per 50) dominion out sepsis with a 94% negative predictive value when obtained 24 and 48 hours later on nascency.12 Glucose levels should also be measured because hypoglycemia tin can be a cause and outcome of respiratory distress.

Full general Handling Principles

• Abstract
• Clinical Presentation
• Diagnosis
• General Treatment Principles
• Etiologies
• References

Treatment of neonatal respiratory distress should be both generalized and disease-specific, and follow updated neonatal resuscitation protocols. Figure ane is an algorithm for the evaluation and management of newborn respiratory distress.eight

Management of Respiratory Distress in Newborns

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Effigy ane.

Suggested algorithm for management of respiratory distress in newborns.

Adapted with permission from Hermansen CL, Lorah KN. Respiratory distress in the newborn. Am Fam Physician. 2007;76(7):992.

RESPIRATORY SUPPORT

Oxygenation can be maintained by delivering oxygen via bag/mask, nasal cannula, oxygen hood, nasal continuous positive airway pressure (N-CPAP), or ventilator back up. Resuscitation with 100% oxygen may increase neonatal bloodshed compared with ambient air.13 Blended oxygen, with the fraction of inspired oxygen ranging from 21% to 50% oxygen, stabilizes premature newborns, and pulse oximetry monitors are used to maintain saturations around 90%.xiv

Noninvasive ventilation, unremarkably using Due north-CPAP, has become the standard respiratory treatment over invasive intubation. N-CPAP has decreased transfers to tertiary care centers with a number needed to care for of 7.3 and a potential toll reduction of $10,000 per case.15 Nasal intermittent positive pressure ventilation tin can also be used. In preterm newborns with RDS, nasal intermittent positive pressure ventilation has been shown to reduce the relative need for mechanical ventilation by 60%.16 Conventional mechanical ventilation is reserved for more severe cases.

SURFACTANT REPLACEMENT

Prophylactic and rescue therapy with natural surfactants in newborns with RDS reduces air leaks and mortality. Neonatal type II pneumocytes produce surfactant in the third trimester to set up for air breathing. Without surfactant, there is higher pulmonary surface tension, atelectasis, and ventilation/perfusion mismatch resulting in hypoxia, hypercapnia, and acidosis.

The minimum required amount of surfactant therapy is 100 mg per kg. An initial dose of 200 mg per kg leads to a statistically significant improvement in oxygenation and decreased demand to retreat, although there is no survival benefit.17,18 A Cochrane review showed that the technique known every bit INSURE (intubate, administrate surfactant, extubate to North-CPAP) led to a 67% relative risk reduction for mechanical ventilation and well-nigh a 50% relative risk reduction for air leak syndromes and progression to bronchopulmonary dysplasia.nineteen The American University of Pediatrics recently released guidelines for surfactant use in newborns with respiratory distress.20

OTHER SUPPORT

Acceptable fluid and electrolyte balance should be maintained. Oral feedings are withheld if the respiratory rate exceeds 60 respirations per minute to prevent aspiration. A neutral thermal environs reduces the newborn's energy requirements and oxygen consumption.21 If the illness exceeds the clinician's expertise and comfort level or the diagnosis is unclear in a critically sick newborn, neonatology should be consulted.

Etiologies

• Abstract
• Clinical Presentation
• Diagnosis
• General Treatment Principles
• Etiologies
• References

The causes of respiratory distress in newborns are summarized in Table iv.8 The post-obit conditions are listed in order of frequency and/or severity.

Table iv.

Summary of Causes of Newborn Respiratory Distress

Cause*	Gestation	Onset	Risk factors	Etiology	Breast radiography findings	Symptom duration
Transient tachypnea of the newborn	Whatever	Firsthand to within two hours of birth	Maternal asthma, male person sex, macrosomia, maternal diabetes mellitus, cesarean commitment	Persistent lung fluid	Hyperexpansion, perihilar densities with fissure fluid, or pleural effusions	Upwards to 72 hours
Respiratory distress syndrome	Preterm	Immediate	Male sexual practice, white race, maternal diabetes	Surfactant deficiency, hypodeveloped lungs	Lengthened footing-glass appearance with air bronchograms and hypoexpansion	Depends on affliction severity
Meconium aspiration syndrome	Term or postterm	Immediate	Meconium-stained amniotic fluid	Lung irritation and obstruction	Fluffy densities with hyperinflation	Depends on disease severity
Infection	Any	Delayed; early onset is i to 3 days, late onset is five to 14 days	Prolonged membrane rupture, maternal fever, grouping B streptococci colonization	Placental transmission or aspiration of infected amniotic fluid (early on onset)	Infiltrates	Depends on disease severity
Pneumothorax	Whatsoever	At onset of pneumothorax	Artificial ventilation	Extrapleural force per unit area exceeding intrapleural pressure	Complanate lung	Depends on disease severity and power to correct
Persistent pulmonary hypertension of the newborn	Any	Within 24 hours	Maternal diabetes, cesarean delivery, black race, maternal obesity, maternal selective serotonin reuptake inhibitor use	Failed physiologic circulatory adaptation	Clear	Depends on disease severity
Congenital heart illness	Whatsoever	Dependent on severity	Genetic abnormalities	Structural abnormality impairing oxygen delivery	Normal or cardiomegaly or pulmonary congestion or effusion if severe	Until corrected
Delayed transition	Term or postterm	Immediate	Sharp commitment	Retained fluid and/or incomplete alveolar expansion	Clear	Minutes to a few hours only

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TRANSIENT TACHYPNEA OF THE NEWBORN

The near mutual etiology of respiratory distress in newborns is TTN, which occurs in about five or vi per 1,000 births.22 It is more common in newborns of mothers with asthma.23 Newborns with TTN accept a greater risk of developing asthma in childhood; in ane study, this clan was stronger in patients of lower socioeconomic status, nonwhite race, and males whose mothers did not have asthma.24 TTN results from delayed reabsorption and clearance of alveolar fluid. Postdelivery prostaglandin release distends lymphatic vessels, which removes lung fluid as pulmonary apportionment increases with the initial fetal breath. Cesarean delivery without labor bypasses this process and is therefore a risk factor for TTN.25 Surfactant deficiency may play a role in TTN. Research indicates a decreased count of lamellar bodies in the gastric aspirate and decreased surfactant phospholipid concentrations in the tracheal aspirate in cases of TTN. Still, treating TTN with surfactant is not indicated.26,27

TTN presents inside ii hours of birth and can persist for 72 hours. Jiff sounds can be clear or reveal rales on auscultation. The higher the respiratory rate at onset, the longer TTN is probable to concluding.28,29 Breast radiography findings (Figure 2 30) support a clinical diagnosis, revealing hyperexpansion, perihilar densities with fissure fluid, or pleural effusions. Blood gases may show hypoxemia, hypercapnia, or respiratory acidosis.

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Figure two.

Chest radiograph of an infant with transient tachypnea of the newborn.

Reprinted with permission from Asenjo Thou. Imaging in transient tachypnea of the newborn. Medscape. http://www.emedicine.com/radio/topic710.htm. Accessed September 14, 2015.

Because TTN is cocky-limited, treatment is supportive. Furosemide (Lasix) may crusade weight loss and hyponatremia, and information technology is contraindicated despite the excess pulmonary fluid nowadays in newborns with TTN.31 Fluid restriction in TTN is beneficial, reducing the elapsing of respiratory support and hospital-related costs.32 Inhaled albuterol reduces tachypnea duration and the need for oxygen therapy, although standardized guidelines are still needed.33 Antibiotics are not indicated in TTN.34 Antenatal corticosteroids given 48 hours before elective cesarean commitment at 37 to 39 weeks' gestation reduce TTN incidence, although information technology is unclear whether delaying cesarean delivery until 39 weeks' gestation is preferable.half-dozen

RESPIRATORY DISTRESS SYNDROME

Newborns born before 34 weeks' gestation may have respiratory distress secondary to surfactant deficiency and lung immaturity. RDS is more common in white males and newborns born to mothers with diabetes mellitus.35,36

RDS symptoms (i.e., tachypnea, grunting, retractions, and cyanosis) occur immediately after birth. Chest radiography (Figure 3 37) shows a diffuse ground-glass appearance with air bronchograms and hypoexpansion, and claret gas measurements prove hypoxemia and acidosis. Symptoms normally worsen in the first 12 to 24 hours. With advances in treatment such every bit surfactant and Northward-CPAP, almost newborns with RDS recover without long-term furnishings. Bronchopulmonary dysplasia tin can occur in complicated cases, leading to recurrent wheezing, asthma, and college infirmary access rates later in life.38

Antenatal corticosteroids given betwixt 24 and 34 weeks' gestation decrease RDS risk with a number needed to treat of 11.39 A single dose of antenatal corticosteroids is beneficial if given more 24 hours before delivery and provides coverage for seven days. The apply of repetitive antenatal corticosteroid doses to prevent RDS is debatable, just no more than ii courses are recommended.40

MECONIUM ASPIRATION SYNDROME

Meconium-stained amniotic fluid is present in approximately 10% to 15% of deliveries, although the incidence of meconium aspiration syndrome is but 1%.41,42 Because meconium excretion frequently represents fetal maturity, meconium aspiration syndrome occurs in term and post-term newborns. Meconium is a conglomeration of desquamated cells, bile pigments, pancreatic enzymes, and amniotic fluid. Although sterile, it can pb to bacterial infection, irritation, obstruction, and pneumonia.

Meconium aspiration syndrome presents at birth as marked tachypnea, grunting, retractions, and cyanosis. Examination may reveal a barrel-shaped breast, with rales and rhonchi heard on auscultation. Breast radiography (Figure 4 37) may show bilateral fluffy densities with hyperinflation. Treatment includes N-CPAP and supplemental oxygen. Ventilator support may be needed in more than severe cases.

Perineal neonatal suctioning for meconium does not prevent aspiration. If the infant is hypotonic at birth, intubation and meconium suctioning are advised. Vigorous infants receive expectant management.43

NEONATAL SEPSIS AND PNEUMONIA

Sepsis tin occur in full-term and preterm infants and has an incidence of one or two per 1,000 alive births.44 Symptoms may brainstorm later in the newborn menses. Risk factors include membrane rupture more than than 18 hours before delivery, prematurity, and maternal fever. Common pathogens include group B streptococci, Escherichia coli, Listeria monocytogenes, Haemophilus influenzae, Staphylococcus aureus, and gram-negative organisms. Universal screening and antepartum antibiotics for group B streptococci carriers reduce early-onset affliction.45 Even so, 5,701 patients demand to be screened and ane,191 patients treated to foreclose one infection.46 A risk reckoner tin can be used to estimate the probability of neonatal early-onset infection.47

Early-onset pneumonia occurs inside the first three days of life, resulting from placental transmission of bacteria or aspiration of infected amniotic fluid. Late-onset pneumonia occurs afterward hospital discharge. Bacterial pathogens are similar to those that cause sepsis.

Serial consummate blood counts, C-reactive protein measurements, and blood cultures assistance with diagnosis and treatment. Intravenous antibiotics are administered if bacterial infection is suspected. Ampicillin and gentamicin are mutual antibiotics for early-onset infections, whereas vancomycin and/or oxacillin with an aminoglycoside are used for tardily-onset infections. Antibiotics should be used judiciously.48 Treatment duration depends on clinical status and laboratory findings.

PNEUMOTHORAX

Pneumothorax occurs if pulmonary space pressure exceeds extrapleural pressure, either spontaneously or secondary to an infection, aspiration, lung deformity, or ventilation barotrauma. Spontaneous pneumothorax occurs in 1% to 2% of term births, and more oft in premature births and in newborns with RDS or meconium aspiration syndrome.49 A modest pneumothorax may be asymptomatic.

Although transillumination can exist helpful, breast radiography confirms the diagnosis. Symptomatic newborns need supplemental oxygen. Tension pneumothorax requires immediate needle decompression or breast tube drainage.

PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN

Frail physiologic mechanisms allow for circulatory transition after nascency with a resultant decrease in pulmonary vascular resistance. Failure of these mechanisms causes increased pulmonary pressures and right-to-left shunting, resulting in hypoxemia. This failure can be caused by meconium aspiration syndrome, pneumonia or sepsis, severe RDS, diaphragmatic hernia, and pulmonary hypoplasia. Astringent persistent pulmonary hypertension of the newborn (PPHN) occurs in two out of 1,000 alive births.l Chance factors include maternal diabetes, cesarean commitment, maternal obesity, and black race. Maternal use of a selective serotonin reuptake inhibitor is associated with the condition. Data bear witness only a small absolute risk.51

With PPHN, respiratory distress occurs inside 24 hours of nascency. On examination, a loud second heart sound and systolic murmur may be heard. Oxygen saturation or PaO₂ increases when 100% oxygen is provided. Echocardiography should be performed to confirm the diagnosis. PPHN is treated with oxygen and other support. In serious cases, ventilator or vasopressor back up and/or apply of pulmonary vasodilators such as inhaled nitric oxide or sildenafil (Revatio) may be helpful. A few cases crave extracorporeal membrane oxygenation.

CONGENITAL Center DEFECTS

Congenital heart defects occur in most i% of births in the United States annually. 1-4th of cases are critical, necessitating surgery in the first year, and one-fourth of those newborns do not survive the outset year.52 Newborns with cyanotic heart disease nowadays with intense cyanosis that is asymmetric to respiratory distress. Cardiac murmur may be heard on examination. Decreases in femoral pulses and lower extremity blood pressures may indicate coarctation of the aorta. Providing 100% oxygen will not better oxygen saturation. Breast radiography and electrocardiography may indicate congenital structural abnormalities, and echocardiography can confirm the diagnosis.

The U.S. Department of Health and Human Services recommends pulse oximetry over physical examination alone to screen for critical congenital heart defects.53 Newborns should be screened before hospital belch, but at least 24 hours after nascency. The cost of treating one critical congenital heart defect exceeds the toll of screening more than than 2,000 newborns, with xx baby deaths prevented with screening.54,55 Pulse oximetry screening for critical congenital center defects is condign standard practice before infirmary belch.

DELAYED TRANSITION

The diagnosis of delayed transition is made retrospectively when symptoms terminate without another identified etiology. It results from retained fluid and incompletely expanded alveoli from a precipitous vaginal delivery, as pathophysiologic mechanisms have not had sufficient time to conform to extrauterine life. Treatment is supportive until the distress resolves a few hours afterward transition concludes.

Example Studies
CASE 1	Instance ii
A male infant was born at 39 3/seven weeks estimated gestational historic period via cesarean commitment because of nonreassuring fetal heart tones. Maternal labor history included clear fluid rupture of amniotic membranes for seven hours. Antenatal screening was negative for group B streptococci. Tachypnea without cyanosis was noted approximately four hours afterward birth. Concrete exam revealed a pulse of 152 beats per minute and respiratory rate of 82 respirations per minute with wet sounding breaths. Mild intercostal retractions were noted. Breast radiography showed increased pulmonary vascularity. A blood glucose measurement was 58 mg per dL (iii.2 mmol per 50). Immature to total neutrophil ratio was 0.12. Oral feedings were held considering of tachypnea, and oxygen was given at ii L by nasal cannula. Over the next 12 hours, the tachypnea decreased to 50 respirations per infinitesimal, and oral feeding was successful. Given the onset of tachypnea and take chances factors (male person sex, non–meconium-stained fluid, and cesarean delivery), this case reflects transient tachypnea of the newborn.	A female person infant was born at 31 five/7 weeks estimated gestational historic period via spontaneous vaginal delivery in the context of placental abruption. The newborn weighed 4 lb, 2 oz and had Apgar scores of 5 and 5. Tachypnea, retractions, and grunting occurred presently after nascency. Physical examination revealed a pulse of 165 beats per minute, respiratory charge per unit of 94 respirations per minute, and claret pressure of 64/44 mm Hg with coarse breath sounds. Claret glucose measurement was 47 mg per dL (2.6 mmol per L), young to full neutrophil ratio was 0.eighteen, and C-reactive protein level was ii.4 mg per L (22.86 nmol per Fifty). Arterial blood gas measurements were pH of seven.25, PCO2 of 65 mm Hg (viii.6 kPa), and PO2 of 40 mm Hg (5.3 kPa). Nasal continuous positive airway pressure level was started immediately, interrupted every bit natural surfactant was administered endotracheally in the commitment room, and resumed while the newborn's temperature was stabilized. The kid was admitted to the neonatal intensive care unit. Given the firsthand onset of tachypnea, this case reflects respiratory distress syndrome. The INSURE (intubate, administer surfactant, extubate to nasal continuous positive airway pressure) technique is emphasized.

Data Sources: A PubMed search was completed in Clinical Queries using the fundamental terms newborn, distress, respiratory, meconium, and tachypnea. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Likewise searched were DynaMed, Clinical Prove, the Cochrane database, Essential Evidence Plus, the National Guideline Clearinghouse database, and the American University of Pediatrics. Search dates: October 2014 to March 2015.

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The Authors

testify all author info

CHRISTIAN L. HERMANSEN, MD, MBA, is senior physician leader of Lancaster (Penn.) General Health, medical director of Downtown Family unit Medicine in Lancaster, and associate manager of the Lancaster General Hospital Family Medicine Residency Program....

ANAND MAHAJAN, MD, is a neonatologist at Lancaster Full general Health'due south Women and Babies Hospital.

Author disclosure: No relevant financial affiliations.

Accost correspondence to Christian Fifty. Hermansen, MD, MBA, Lancaster Full general Hospital, 555 North Knuckles St., Lancaster, PA 17602 (e-mail: clherman@lghealth.org). Reprints not available from the authors.

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