Evaluating and Treating Respiratory Distress

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Evaluating and Treating Respiratory Distress
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Respiratory Distress is a symptom of

• TTN (transient tachypnea of the newborn)
• RDS (premature lungs)
• Meconium aspiration
• pneumothorax
• Congenital heart disease
• Diaphragmatic hernia
• Sepsis/pneumonia
• Metabolic acidosis/metabolic disease

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TTN/ transient tachypnea of the newborn

• Also known as RDS type 2 or wet lung syndrome
• Benign and self limited process
• It occurs in about 11 per 1,000 live births more
  common in boys, in infants delivered by CS,
  infants with perinatal asphyxia, umbilical cord
  prolapse
• Characterized by tackypnea and sometimes hypoxia
• diffuse parenchymal infiltrates on CXR, a "wet
  silhouette" around the heart, or accumulation of
  fluid in the various intralobar spaces giving the
  CXR of fluffy appearance. The lungs usually are
  affected diffusely

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Cause of TTN

• It is thought that slow absorption of the fluid
  in the fetal lungs causes TTN. This fluid makes
  taking in oxygen harder and the baby breathes
  faster to compensate.

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Symptoms of TTN

• rapid breathing rate (over 60 breaths/minute)
• grunting sounds with breathing
• flaring of the nostrils
• retractions (pulling in at the ribs with
  breathing)

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Diagnoses of TTN

• Chest x-rays are often used to help diagnose TTN.
  On x-ray, the lungs show a streaked appearance
  and appear over-inflated.
• However, it may be difficult to tell whether the
  problem is TTN or hyaline membrane disease or
  pneumonia.
• Often, TTN is diagnosed when symptoms suddenly
  resolve by the third day of life.

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treatment

• Always self resolving
• Supportive treatment
• Diagnosis not definitive until it resolves

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RDS/Respiratory Distress Syndrome

• Generally occurs in premies, but can have late
  RDS
• Increasing with increased incidence of premature
  birth
• Risk factors in late preterm infants include -
  maternal diabetes, multiple birth, cesarean
  section prior to the onset of labor, perinatal
  asphyxia, cold stress, and infants whose siblings
  suffered from RDS.
• RDS, also called HMD or hyaline membrane disease,
  is one of the most common problems of premature
  babies. The course of illness withRDS depends on
  the size and gestational age of the baby, the
  severity of the disease, whether or not a baby
  has a patent ductus arteriosus and whether or not
  the baby needs mechanical help to breathe.
• RDS typically worsens over the first 48 to 72
  hours, then improves with treatment.

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What causes HMD?

• RDS occurs when there is a deficiency of
  surfactant.
• Surfactant consists of phospholipids and protein.
  It begins to be produced at about 24-28 weeks of
  pregnancy. Surfactant is found in amniotic fluid
  between 28 and 32 weeks. By about 35 weeks
  gestation, most babies have adequate amounts of
  surfactant.
• Surfactant is normally released into the lung
  tissues where it helps lower surface tension in
  the airways. This helps keep the lung alveoli
  open. When there is not enough surfactant, the
  alveoli collapse. As the alveoli collapse,
  damaged cells collect in the airways, creating a
  hyaline membrane.
• RDS occurs in over half of babies born before 28
  weeks gestation, but only in less than one-third
  of those born between 32 and 36 weeks.

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Other risk factors for RDS

• Caucasian or male babies
• previous birth of baby with RDS
• cesarean delivery
• perinatal asphyxia/cold stress (suppresses
  surfactant production)
• perinatal infection
• multiple gestation
• infants of diabetic mothers
• babies with patent ductus arteriosus

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What are the symptoms of HMD?

• respiratory difficulty at birth that gets
  progressively worse
• cyanosis
• flaring of the nostrils
• tachypnea
• grunting sounds with breathing
• retractions

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How is HMD diagnosed?

• appearance, color, and breathing efforts.
• Risk factors
• chest x-rays of lungs - often show a unique
  "ground glass" appearance called a
  reticulogranular pattern.
• blood gases low PaO2 and increase CO2 often
  with acidosis

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Levels of support

• Hood oxygen
• High flow nasal canula
• CPAP
• Mechanical ventilation
• Surfactant replacement this is most effective
  if started in the first six hours of birth.
  Surfactant replacement has been shown to reduce
  the severity of HMD. Surfactant is given as
  prophylactically for babies at high risk for HMD.
  For others it is given as a "rescue" medication.

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Indications for surfactant

• RDS requiring greater than 40 FIO2
• hypercarbia
• a/A gradient lt 0.36

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a/A gradient

• Can be helpful in determining if a baby would
  benefit from Surfactant therapy.
• Calculated indices of lung function (such as the
  arterial to Alveolar (a/A) oxygen tension ratio)
  predict the severity and outcome of respiratory
  failure more accurately than looking at the FiO2
  alone.
• how to calculate the arterial/Alveolar oxygen
  tension ratio
• FiO2 measured from headbox, CPAP, or vent (not
  accurate from nasal canula).
• The simplified equation looks like this
• a/A Ratio PaO2 / (FiO2 x 720) (PCO2 x
  1.25).
• (the 720 is 593 in Denver)
• A normal a/A ratio is 0.75. As lung disease
  worsens, the a/A ratio will decrease. It is well
  accepted that infants with RDS and an a/A ratio
  less than 0.22 should receive surfactant. A
  recent study found that infants with RDS and an
  a/A ratio less than 0.36 will benefit from
  surfactant.

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Complications of HMD

• pneumomediastinum
• pneumothorax
• pneumopericardium
• pulmonary interstitial emphysema (PIE) - air
  leaks and becomes trapped between the alveoli,
  the tiny air sacs of the lungs.
• chronic lung disease or bronchopulmonary
  dysplasia

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MAS/meconium aspiration syndrome

• 13 of all infants have MSAF
• About 5 of these develop MAS
• 50 require mechanical ventilation and mortality
  is about 5-10
• Can result in severe respiratory distress
  requiring mechanical ventilation, surfactant,
  iNO, ECMO
• Suctioning on the perineum and routine tracheal
  suctioning ??

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Symptoms of MAS

• MAS is characterized by early onset of
  respiratory distress (within 2 hours) in a
  meconium-stained infant.
• Tachypnoea, cyanosis and hyperinflation are the
  main clinical findings.
• Radiologically the typical progression is from
  global atelectasis in early X-rays to a
  widespread patchy opacification accompanied by
  areas of hyperinflation and/or atelectasis.
• Blood gas shows hypoxia, accompanied by
  hypercarbia in those infants with significant
  airway obstruction or severe respiratory failure.

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Treatment of MAS

• oxygen is critically important in infants with
  MAS, and in many infants is the only therapy
  needed. The pulmonary vasculature in the term
  infant is very sensitive to oxygen tension, and
  failure to maintain good sats can lead to
  pulmonary hypertension. Give oxygen early and
  liberally in any baby with potential MAS. Target
  range for oxygen saturation is 94-98 target
  PaO2 60 90 mm Hg.
• Nasal CPAPConsider as additional support for
  infants with MAS where there is moderate
  respiratory distress and hypoxia.
• Intubation and positive pressure
  ventilationIndicationsPersistent hypoxia (SaO2
  lt 90, PaO2 lt 50) in 100 oxygenRespiratory
  acidosis with pH lt 7.20

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pneumothorax

• Risk factors include MSAF, use of PPV,
  respiratory distress, prematurity
• Can occur spontaneously
• If non-symptomatic treatment is just observation
• If respiratory distress, needle the air and
  consider chest tube

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Signs of a pneumothorax

• Acute decompensation with increasing respiratory
  distress, including rapid breathing, grunting,
  nostril flaring, and chest wall retractions
• difficulty hearing breath sounds
• change in the location of heart or lung sounds
  when the organs are moved by the presence of air
• changes in arterial blood gas levels

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Pneumonia/sepsis

• 90 of infants will have tachypnea or other
  respiratory symptoms as part of their clinical
  presentation.
• Risk factors include GBS, preterm delivery,
  maternal chorio, prolonged ROM
• Occurs because of interuterine infection (i.e.
  cytomegalic inclusion virus) or shortly after
  birth.
• Virus can be principle cause although other
  organism such as strep, staph or E Coli. Common
  viral pneumonias include H. flu and herpes.
• X-ray - patchy infiltrate in perihilar area. May
  lead to diffuse involvement of entire lungs.
  Occasionally pleural effusion may occur.
• Complications - generalized sepsis or lung
  abscess may occur.

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CDH/congenital diaphragmatic hernia

• developmental abnormality of the diaphragm
  resulting in a defect that permits abdominal
  viscera to enter the chest
• 1 in 3,000 live births
• Males gt females
• Mortality approaches 50

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CDH treatment

• NG/OG to suction for decompression
• Early intubation avoid BMV or CPAP

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CHD/Congenital Heart Disease

• Differentiate between heart and lung
• Reponse to oxygen
• Hyperoxyia challenge
• PaO2
• 300 normal
• 150-300 think lung disease
• lt150 think cardiac or PPHN
• CXR

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ETC.

• "THE MISFITS"
• T-Trauma (nonaccidental and accidental)
• H-Heart disease/hypovolemia/hypoxia
• E-Endocrine (congenital adrenal hyperplasia,
  thyrotoxicosis)
• M-Metabolic (electrolyte imbalance)
• I-Inborn errors of metabolism Metabolic
  emergencies
• S-Sepsis (meningitis, pneumonia, urinary tract
  infection)
• F-Formula mishaps (under- or overdilution)
• I-Intestinal catastrophes (volvulus,
  intussusception, necrotizing enterocolitis)
• T-Toxins/poisons
• S-Seizures

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Cheap metabolic work up

• Glucose
• Bicarb
• Ammonia
• Urine ketones