1-tachypnea (RR>60/min)

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Respiratory distress

• 1-tachypnea (RRgt60/min)
• 2-retraction ( subcostal intercostal
  suprasternal ) ? WOB
• 3-grunting
• 4-flaring of ala nasi
• 5-cyanosis
• 6-rales and wheezing

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Respiratory distress

• Time of onset?
• Cyanosis response to oxygen?
• Chest X ray?

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RDS risk factors

• prematurity,
• maternal diabetes
• perinatal asphyxia,
• twin pregnancy,
• cold stress,
• precipitous labor,
• cesarean delivery.
• The incidence is highest in preterm male
• or white infants.

4
Reduced risk of RDS

• The risk of RDS is reduced in pregnancies with
• chronic or pregnancy-associated hypertension,
• maternal heroin use,
• prolonged rupture of membranes, and
• antenatal corticosteroid prophylaxis.

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Pathophysiology

• lack of surfactant leads to progressive
  atelectasis,
• V/Q mismatch, hypoxia, hypercapnia, respiratory
  and metabolic (lactic) acidosis, pulmonary
  hypertension, right to left shunting through
  ductus arteriosus and foramen ovale.

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Pathology

• the lungs of infants who die of RDS have a
  characteristic uniformly ruddy and airless
  appearance macroscopically resembling hepatic
  tissue. On microscopic examination the prominent
  finding is diffuse atelectasis and hyaline
  membrane.

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Surfactant Therapy Animal Models

• Expansion patterns in lung sections of a newborn
  rabbit
• 1a - after treatment with natural surfactant
• 1b - no treatment

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Radiographic Changes WithExogenous Surfactant
Treatment

• before

• after

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Air bronchogram - ground glass apearance -
hypoinflation
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Survanta
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• Surfactant is present in high concentrations in
  fetal lung homogenates by 20 wk of gestation, but
  it does not reach the surface of the lungs until
  later.
• It appears in amniotic fluid between 28 and 32
  wk.
• Mature levels of pulmonary surfactant
• are usually present after 35 wk.
• Synthesis of surfactant depends in part on normal
  pH, temperature, and perfusion.
• Asphyxia, hypoxemia, and pulmonary
• ischemia, particularly in association with
  hypovolemia, hypotension,and cold stress, may
  suppress surfactant synthesis.

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Clinical manifestations

• infants with RDS present at birth or within
  several hours after birth with clinical signs of
  respiratory distress including tachypnea,
  retraction, grunting, nasal flaring and cyanosis.
• A late onset of tachypnea should suggest other
  conditions.

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Clinical manifestations

• Some patients require resuscitation at birth
  because of intrapartum asphyxia or initial severe
  respiratory distress (especially with a
  birthweight lt1,000 g).
• Cyanosis is relatively unresponsive to oxygen
  administeration.

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Clinical manifestations

• The natural course of untreated RDS is
  characterized by progressive worsening of
  cyanosis and dyspnea. If the condition is
  inadequately treated, blood pressure may fall
  fatigue, cyanosis, and pallor increase, and
  grunting decreases or disappears as the condition
  worsens. Apnea and irregular respirations occur
  as infants tire and are ominous signs requiring
  immediate intervention. Patients may also have a
  mixed respiratory- metabolic acidosis, edema,
  ileus, and oliguria. Respiratory failure may
  occur in infants with rapid progression of the
  disease.

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Clinical manifestations

• In most cases, the symptoms and signs reach a
  peak within 3 days, after which improvement is
  gradual. Improvement is often heralded by
  spontaneous diuresis and the ability to oxygenate
  the infant at lower inspired oxygen levels or
  lower ventilator pressures.
• Death is rare on the 1st day of illness, usually
  occurs between days 2 and 7, and is associated
  with alveolar air leaks (interstitial emphysema,
  pneumothorax), pulmonary hemorrhage, or IVH.
• Mortality may be delayed weeks or months if BPD
  develops in mechanically ventilated infants with
  severe RDS.

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Chest X Ray

• the typical radiographic features (not
  pathognomonic) consist of a diffuse
  reticulogranular pattern giving the classic
  ground-glass appearance in both lung fields
  with superimposed airbronchograms and
  hypoaeration of the lung.

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Differential diagnosis

• in pneumonia manifested at birth, the chest
  roentgenogram may be identical to that for RDS.
  Maternal group B streptococcal colonization,
  organisms on Gram stain of gastric or tracheal
  aspirates or a buffy coat smear, and/or the
  presence of marked neutropenia may suggest the
  diagnosis of early-onset sepsis.
• Cyanotic heart disease (total anomalous pulmonary
  venous return) can also mimic RDS both clinically
  and radiographically. Echocardiography with color
  flow imaging should be performed in infants who
  fail to respond to surfactant replacement to rule
  out cyanotic congenital heart disease as well as
  ascertain patency of the ductus arteriosus and
  assess pulmonary vascular resistance.

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Differential diagnosis

• Persistent pulmonary hypertension, aspiration
  (meconium, amniotic fluid) syndromes, spontaneous
  pneumothorax, pleural effusions, and congenital
  anomalies such as cystic adenomatoid
  malformation, pulmonary lymphangiectasia,
  diaphragmatic hernia, and lobar emphysema must be
  considered, but can generally be differentiated
  from RDS by roentgenographic evaluation.

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PREVENTION

• Avoidance of unnecessary or poorly timed cesarean
  section, appropriate management of high-risk
  pregnancy and labor, and prediction and possible
  in utero acceleration of pulmonary immaturity are
  important preventive strategies.
• In timing cesarean section or induction of
  labor, estimation of fetal head circumference by
  ultrasonography and determination of the lecithin
  concentration in amniotic fluid by the
  lecithinsphingomyelin ratio
• (particularly useful with phosphatidylglycerol in
  diabetic pregnancies)
• decrease the likelihood of delivering a premature
  infant.
• Antenatal and intrapartum fetal monitoring may
  similarly decrease the risk of fetal asphyxia
  asphyxia is associated with an increased
  incidence and severity of RDS.

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PREVENTION

• Administration of betamethasone to women 48 hr
  before the delivery of fetuses between 24 and 34
  wk of gestation significantly reduces the
  incidence, mortality, and morbidity of RDS.
• Corticosteroid administration is recommended for
  all women in preterm labor (24-34 wk gestation)
  who are likely to deliver a fetus within 1 wk.

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PREVENTION

• Prenatal glucocorticoid therapy decreases the
  severity of RDS and reduces the incidence of
  other compiications of prematurity, such as IVH,
  patent ductus arteriosus (PDA), pneumothorax, and
  necrotizing enterocolitis, without adversely
  affecting postnatal growth, lung mechanics or
  development, or the incidence of infection.
• Prenatal glucocorticoids may act synergistically
  with postnatal exogenous surfactant therapy.

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PREVENTION

• Prenatal dexamethasone may be associated with a
  higher incidence of periventricular leukomalacia
• than betamethasone.
• The relative risk of RDS, IVH and death is higher
  with antenatal dexamethasone treatment when
  compared with betamethasone..
• Administration of a 1st dose of surfactant into
  the trachea of symptomatic premature infants
  immediately after birth (prophylactic) or during
  the 1st few hours of life (early rescue) reduces
  air leak and mortality from RDS, but does not
  alter the incidence of BPD.

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Treatment

• The basic defect requiring treatment is
  inadequate pulmonary exchange of oxygen and
  carbon dioxide metabolic acidosis and
  circulatory insufficiency are secondary
  manifestations.

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Treatment

• For the 1st 24 hr, 10 glucose and water should
  be infused through a peripheral vein at a rate of
  65-75 ml/kg/24 hr.
• Excessive fluids (gt140 cc/kg/day) contribute to
  the development of PDA and BPD.

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Goal ABG

• pao255-70,
• paco245-55 and
• pH7.25- 7.45

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Antibiotics should be started,

• Because
• pneumonia may present with the same clinical and
  radiological signs.

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Dopamine

• should be started
• at 5-10mcg/kg/min
• to support circulation in the case of
  hypotension. Relief of metabolic and respiratory
  acidosis by bicarbonate and assisted ventilation
  may cause a fall in blood pressure.

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Surfactant

• 1- 3 doses of intratracheal surfactant in the
  first 48 hr of life .
• The earlier the administration , the better the
  result.

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Respiratory support

• The goal of respiratory support is establishment
  of appropriate oxygen saturation (90 -95) and
  ABG .
• Different levels of respiratory care
• 1- oxygen via oxyhood
• 2-oxygen via nasal pronge
• 3- nasal CPAP
• 4- intubation and mechanical ventilation

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• Nasal prong

• Oxyhood

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• Nasal CPAP

• Oxygen mask

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Respiratory failure

• PHlt 7.2
• PaCO2gt 60 mmHg
• PaO2lt 50 mmHg
• or
• Frequent apnea
• Despite inspiring 100 O2.

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Other causes of respiratory distress

• 1-pneumonia
• 2-meconium aspiration
• 3- transient tachypnea of newborn
• 4-TE fistula
• 5-diaphragmatic paralysis
• 6-vocal cord paralysis
• 7-congenital diaphragmatic hernia
• 8- cystic adenomatoid malformation
• 9-bronchogenic cyst
• 10-congenital lobar emphysema
• 11-congenital heart disease
• 12-pulmonary lymphangiectasis
• 13- pneumothorax
• 14-PPHN
• 15-choanal atresia
• 16-pulmonary hypoplasia
• 17-pulmonary sequestration