Respiratory Distress in Newborn
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Transcript of Respiratory Distress in Newborn
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Respiratory Distress in Newborn
Part 2 by Yong
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Transient Tachypnea of Newborn
(TTN)
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Most common cause of respiratory distress. 40% cases. Residual fluid in fetal lung tissues. Risk factors- maternal asthma, c- section,
macrosomia, maternal diabetes
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The infant become tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress.
They are neurologically normal, symptoms can last few hours to two days.
The pathophysiological mechanism is the delayed resorption of fetal lung fluid which eventually clears over the next several hours to days.
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Hyperinflation with clear lung parenchyma Perihilar linear densities Fluid in the fissures Laminar effusions Fuzzy vessels
There should be no areas of consolidation .
Chest radiographs
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Congenital pneumonia
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• Intrauterine infection or during delivery• Most are bacterial in origin Pneumonia that becomes clinically
evident within 24 hours of birth may originate at 3 different times.
The 3 categories of congenital pneumonia are as follows:
◦ True congenital pneumonia◦ Intrapartum pneumonia◦ Postnatal pneumonia
pathophysiology
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True congenital pneumonia is already established at birth.
Transmission of congenital pneumonia usually occurs via 1 of 3 routes: ◦ Hematogenous◦ Ascending◦ Aspiration
True congenital pneumonia
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• Intrapartum pneumonia is acquired during passage through the birth canal.
• It may be acquired via hematogenous or ascending transmission: – from aspiration of infected or contaminated
maternal fluids – from mechanical or ischemic disruption of a
mucosal surface that has been freshly colonized with a maternal organism
Intrapartum pneumonia
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Postnatal pneumonia in the first 24 hours of life originates after the infant has left the birth canal.
It may result from some of the same processes described above, but infection occurs after the birth process.
Postnatal pneumonia
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Group B Streptococcus (GBS) Nontypable Haemophilus influenzae cytomegalovirus, Treponema pallidum,
Toxoplasma gondii, Enterococci
Etiology
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Afebrile Marked respiratory distress Tachypnea Metabolic acidosis Septicemia and shock
Clinical Findings
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Chest radiographs
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Meconium aspiration syndrome
(MAS)
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Incidence- 1.5- 2 % in term or post term infants.
Meconium is locally irritative, obstructive & medium for for bacterial culture
Meconium aspiration causes significant respiratory distress. Hypoxia occurs because aspiration occurs in utero.
Thick meconium could block air passages and cause atelectasis and air leak syndromes
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The baby with MAS is usually post-term or small-for-date.
There may be meconium staining of the umbilical cord, nails and skin.
The chest may be hyperinflated and onset of distress is usually within the first 4-6 hours.
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• Diffuse “ropey” densities• Patchy areas of atelectasis and emphysema
from air-trapping• Hyperinflation of lungs• No air bronchograms
• Clearing usually quick if mostly water; days-weeks if mostly meconium
Chest radiographs
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Respiratory Distress Syndrome
(Hyaline Membrane Disease)(RDS)
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Most common cause of respiratory distress in prematurity, asphyxia and maternal diabetes infants, correlating with structural & functional lung immaturity.
Prolonged rupture of membranes and intrauterine growth retardation are believed to enhance lung maturity.
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Surfactant is needed to decrease alveolar surface tension and keep them open.
In a preterm baby, absence of surfactant leads to alveolar collapse during expiration.
This affects gas exchange and the baby goes into respiratory failure
Pathophysiology
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Diagnosis of respiratory distress should be suspected when grunting, retraction or other typical distress symtoms occur in premature infant.
Symptoms present in first 2 hours of life◦ Symptoms that begin > 8 hrs are not due to HMD
May turn in severity from 24 - 48 hours Then, gradual improvement > 48-72 hours
Clinical Findings
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• X-ray showing air bronchogram and hazy lung suggestive of HMD. –mild disease: reticulo-granular pattern – severe disease: "white out" picture
• Typically, diffuse “ground-glass” or finely granular appearance
• Bilateral and symmetrical distribution • Air bronchograms are common, especially
extending peripherally• “Granularity” is the interplay of:
• Air-distended bronchioles & ducts• Background of atelectasis of alveoli
Chest radiographs
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Classic respiratory distress syndrome (RDS). Bell-shaped thorax is due to generalized underaeration. Lung volume is reduced, the lung parenchyma
has a diffused reticulogranular pattern, and peripherally extending air bronchograms are present.
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Moderately severe respiratory distress syndrome (RDS). The reticulogranular pattern is more prominent and uniformly
distributed than usual. The lungs are hypoaerated. Increased air bronchograms are observed
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Severe respiratory distress syndrome (RDS). Reticulogranular opacities are present throughout both lungs, with prominent air bronchograms and total
obscuration of the cardiac silhouette.
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Treatment
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Rx is supportive because the condition is usually self limited.
Prenatal administration of steroids 48hrs before elective C- section @ 37- 39 weeks gestation reduces TTN but this has not common practice.
Transient Tachypnea of Newborn
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IV C Penicillin 50000unit/kg 6hly IV Gentamycin 4mg/kg daily
Congenital Pneumonia in newborn
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General intervention for oxygenation. Prenatal administration of corticosteroids
between 24- 34 wks gestation reduces risk of respiratory distress when risk of preterm delivery is high.
Post natal steroids may decrease mortality but may increase risk of cerebral palsy.
Respiratory distress Syndrome
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• Antenatal steroids will prevent the occurrence and severity of RDS in preterm babies between 24 and 34 weeks of gestation.
• Optimal effect of antenatal steroids is seen if delivery occurs after 24 hours of the initiation of therapy. Effect lasts for 7 days.
Antenatal corticosteroids
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If delivery is anticipated below 34 weeks of gestation.
Dose recommended is:◦ Inj Betamethasone 12 mg 1M every 24 hrs x 2
doses; or ◦ Inj Dexamethasone 6 mg 1M every 12 hrs x 4
doses. ◦ Multiple courses of antenatal steroids are not
beneficial and hence are not recommended
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surfactant therapy should be instituted only if there are facilities for ventilation.
The efficacy of surfactant in reducing the duration of ventilation is proven.
Prophylactic surfactant use is recommended for any neonate< 28 weeks and < 1000 gms.
Surfactant therapy
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• Choice of drugs:1. Survanta – 100mg of phospholipids/kg/dose (4mL/kg)– Repeat > 6H after the previous dose if the
infant remains intubated and requires at least 30% O2 to maintain PaO2 <80mmHg
2. BLES– 135mg phospholipids/kg/dose (5mL/kg)– Repeat up to 3 times within the 5 post natal
days if difficult to maintain oxygenation