NEONATAL PULMOMARY DISORDERS

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NEONATAL PULMOMARY DISORDERS
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RESPIRATORY DISTRESS SYNDROME

• AKA Hyaline Membrane Disease
• Occurs more often in boysmore often in whites
  than non-whites
• Associated with
• Infants less than 37 wks gestationthe preemier
  the baby, the greater the risk
• Infants of diabetic mothers
• Multiple births
• C-section prior to onset of labor
• Cold stress
• Siblings who had RDS

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RDS - Etiology

• A deficiency of surfactant and abnormal lung
  surface tensionscar tissue replaces alveolar
  tissue
• Insufficient surfactant as well as immature cell
  and vascular development of the lungs
• At about 16 wks gestation, alveolar type II cells
  synthesize and store surfactantincreasing
  amounts are produced as the fetus approaches term
• Between weeks 28-38, surfactant is secreted into
  the alveoli and migrates into the amniotic fluid
  thru the trachea and esophagus
• Primitive alveoli form between wks 27-35, with
  true alveoli forming between wks 30-36
• Infants born before week 28 have structural
  underdevelopment of the terminal airspaces with
  little to no surfactant

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RDS-Etiology, cont

• Surfactant deficiency along with the extremely
  compliant chest wall of the preterm infant
  results in an increase in surface forces and lung
  elastic recoil
• This leads to atelectasis, decreased FRC,
  decreased C, increased Raw, and V/Q mismatch
  resulting in hypoxia, hypercarbia, and
  respiratory acidosis
• The pulmonary arteries constrict, reducing blood
  flow and damaging the cells that line the alveoli
• Immature surfactant is affected by hypoxemia,
  hypothermia, and acidosisall are common in
  preemies
• Within 2 days of birth, immature lungs begin to
  mature while true alveoli and capillaries
  continue to develop in the lung
• Chronic stress has a protective influence
  conditions such as maternal heroin use and
  toxemia are thought to induce surfactant
  productionpremature rupture of the membranes for
  gt24 hrs also has a protective effect

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RDS Clinical Presentation

• Infant is usually preterm
• Tachypnea and labored breathing
• Grunting attempting to maintain the FRC
• Nasal flaring
• Retractions high insp pressures distort the
  chest wall instead of inflating the stiff lungs
• May be hypotonic and unresponsive
• ABG is usually mixed acidosis with hypercarbia
  and hypoxemia

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RDS on CXR

• CXR shows diffuse, fine reticulogranular
  densities (ground glass)
• Stage I fine diffuse reticulogranular pattern
• Stage II more dense lung/air bronchograms w/i
  heart border
• Stage III even more dense/air bronchograms all
  over
• Stage IV white out

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RDS Disease Progression

• Mild cases peak in about 72 hours, then a gradual
  improvementfirst sign of improvement is
  spontaneous diuresis
• Infants with severe RDS die in 2-7 days with
  death most often associated with PIE,
  pneumothorax, or IVH

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RDS - Diagnosis

• Based on history, clinical presentation, CXR, and
  lab values
• LS Ratio Lecithin (dipalmitoylphosphatidyl
  choline) is the most abundant lipid found in
  surfactantwhen the lung is mature, there is
  twice as much lecithin as sphingomyelinan LS
  ratio of 21 is evidence of lung maturity and a
  low risk for RDS
• PG level phosphatidylglycerol is the 2nd most
  abundant phospholipid in surfactant but isnt
  made until about week 35the presence of PG in
  amniotic fluid indicates a low risk for RDS
• Foam test/Shake test amniotic fluid is mixed
  with alcohol and shakenif theres surfactant
  present, foam will appear that will last for
  several hoursif theres no surfactant, no foam
  appears or it will appear only briefly

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RDS - Treatment

• Prevention delay premature delivery as long as
  possible (terbutaline/albuterol) give
  glucocorticoids at least 2 days prior to delivery
  to accelerate lung development and promote
  surfactant secretion
• Surfactant replacement can reduce the time on
  mechanical ventilation and pressure/oxygen
  requirements
• CPAP/Mechanical Ventilation

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RDS

• Respiratory Management
• Maintain adequate alveolar ventilation without
  causing lung damage
• Use of pressure rather than volume ventilation
• Maintain acceptable ABGs
• Early intervention may reduce total support
  needed
• Other
• Adequate hydration, fluid balance, electrolytes
• thermoregulation

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RDS

• Complications
• IVH
• More common in small babies
• PPV is transmitted to the cranium causing vessel
  rupture
• Barotrauma
• Pneumothorax
• subQ
• DIC
• Patient throws a bunch of clots that uses up the
  clotting factors
• Result is a tendency to bleed profusely
• PDA hypoxemia keeps the ductus open

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Transient Tachypnea of the Newborn

• AKA RDS Type II and wet lung syndrome
• More common in males and in term infants,
  especially after C-section
• Etiology thought to be due to delayed
  absorption of fetal lung fluid by the lymphatics
• Results in decreased compliance, decreased tidal
  volume/increased rate, and increased dead space

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TTNB Clinical Presentation

• Usually has good Apgar scores
• Tachypnea (60-160/min), cyanosis, grunting,
  flaring, and retractions begin within a few
  hourssymptoms are nearly identical to RDS
• CXR shows pulm vascular congestion, prominent
  perihilar streaking, fluid in the interlobular
  fissures, hyperexpansion, and a flat diaphragm

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TTNB - Diagnosis

• Similar in presentation to RDS, group B
  streptococcal pneumonia, and PPHN
• Usually diagnosed after these are ruled out
• Usually resolves after about 24 hours of O2
  therapy
• Evaluate for infection since sepsis and pneumonia
  present similarly

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TTNB - Treatment

• O2/CPAP supplemental oxygen usually only needed
  for about 24-48 hrs
• Frequent position changes help prevent further
  retention of fluid
• Bottle feedings are postponed until the tachypnea
  resolves to prevent aspiration

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BPD

• BPD bronchopulmonary dysplasia
• Most cases follow treatment of RDS
  specifically, mechanical ventilation
• Sort-of like baby COPD

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BPD

• Pathophysiology 4 factors lead to BPD
• Oxygen toxicity
• High FiO2 leads to edema and thickening of the
  alveolar-capillary membrane
• Alveolar tissue hemorrhages and becomes necrotic
• Interstitial spaces become fibrotic
• Barotrauma from high pressures/long It
• Presence of a PDA pulm congestion increases
  pressure/FiO2 requirements of ventilator
• Fluid overload pulmonary edema
• Studies show babies with BPD have antisurfactant
  protein A antibodies and decreased ability to
  secrete cortisol

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BPD

• Diagnosis
• Chronic O2/Ventilator support
• CXR
• Stage 1 RDS ground glass
• Stage 2 granular infiltrates
• Stage 3 multiple small cysts
• Stage 4 large, irregular cysts
• ABG like a chronic lungers
• EKG RAD with RVH
• PFT increased Raw

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BPD

• Treatment
• Prevention avoid high pressures/FiO2
• Mechanical ventilation
• Allow a small leak around ETT to avoid stenosis
• Trach if more than 1 month or so on vent
• High frequency ventilation
• Adequate humidification have thick secretions
• Resp Care Modalities
• CPT
• Sx
• Bronchodilators probably not effective as not
  much bronchial smooth muscle present

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BPD

• Treatment, cont
• Fluid
• Use diuretics/fluid restriction to control pulm
  edema
• Watch electrolyte balance
• Right heart failure
• Diuretics and digoxin
• Chemically or surgically close the PDA
• Nutrition
• Have to meet metabolic needs as well as needs for
  growth
• Inadequate nutrition delays growth and may make
  weaning more difficult
• Too many calories, though, increases VO2 and VCO2
• Vitamin E
• Vitamin E deficiency increases incidence of O2
  toxicity
• Administration of Vit E decreases lung injury
  from O2 toxicity
• No conclusive evidence that Vit E decreases the
  incidence of BPD, though

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ROP

• Physiology
• Capillaries of the retina begin forming at 16 wks
• Capillaries start growing out from the optic
  nerve and grow towards the retina
• They dont reach the retina until about 40 wks

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ROP

• Pathophysiology
• Retinal vessels constrict with PaO2 is high
• These vessels can then necrose
• The ones that havent necrosed proliferate to try
  and establish a blood supply to the retina
• The new vessels can extend too far and cause the
  retina to detach
• Risk factors immaturity, hyperoxia, hypoxia,
  blood transfusions, IVH, apnea, infection,
  hypercarbia, PDA, vit E deficiency, lactic
  acidosis, prenatal complications, use of
  Indomethicin

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ROP

• Diagnosis
• Opthalmic examination of the internal eye is
  required
• Only takes 15-20 minutes of hyperoxia to start
  ROP
• May take several weeks to progress through the
  stages
• Not all babies progress to stage 5

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ROP

• Treatment
• Prevention Keep PaO2 lt100
• cryotherapy
• This basically freezes the retina preventing
  abnormal blood vessel growth
• Can scar and cause retinal detachment
• Laser therapy
• Lasers are used to coagulate the retina, again
  stopping abnormal vessel growth
• Vitrectomy (removing vitreous part of eye) and
  lensectomy (removing the lens of the eye) are
  surgical treatments

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INTRAVENTRICULAR HEMORRHAGE

• AKA Intracranial hemorrhage
• Intracranial bleeds are common in preemies and
  are also common in term babies with birth trauma
• In term infants, the choroid plexus (hypothalamus
  area of the brain) is the most common site of
  bleed
• In preemies, its the subependymal region, closer
  to the cerebellum
• The inability to regulate blood flow is the usual
  cause

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IVH

• Blood flow fluctuates with shock, acidosis,
  hypernatremia, blood transfusions, seizures, and
  rapid infusions
• Mechanical ventilation and Trendelenberg position
  increase ICP and can trigger hemorrhage
• Babies of alcoholic mothers have a much higher
  incidence of IVH
• See the list of risk factors on page 308

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IVH

• Signs/Symptoms
• Apnea
• Hypotension
• Drop in hematocrit
• Flaccidity
• Bulging fontanelles
• Tonic posturing
• There are 4 grades of IVHthe bigger the number,
  the more extensive the bleed

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IVH

• Complications
• Posthemorrhagic hydrocephalus
• Caused by obstruction of CSF and impairment of
  CSF absorption
• Use lumbar puncture to draw off CSF to keep ICP
  down
• May have to place a ventricular-peritoneal shunt,
  which drains CSF into peritoneal cavity
• Ventriculostomy is a catheter into the brain that
  can be used to drain CSF externally

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IVH

• Treatment
• The best treatment is avoidance minimize the
  risk factors as much as possible
• Besides shunts, osmotic agents that concentrate
  the blood can be used to draw the fluid from the
  cells back into the blood vessels

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Asphyxia/Apnea

• Asphyxia is a combination of hypoxia,
  hypercarbia, and acidosis in the fetus or
  neonatecan start as a lack of oxygen or can be
  from a drop in perfusion
• Placental insufficiency in utero is most common
  cause of fetal asphyxia but any maternal or cord
  problem that interferes with gas exchange will
  lead to asphyxia (see table 10-4/pg 311)

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Apnea of Prematurity

• Cessation of breathing effort for gt20 seconds OR
  any pause long enough to cause bradycardia or
  cyanosis or both
• Not to be confused with periodic breathing (short
  pauses followed by an increased RR)
• The most common form of infant apnearelated to
  CNS immaturity/ dysfunction
• Linked to thermal instability, metabolic
  disorders, PDA, shock, anemia, sepsis, and NEC

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Apnea - Etiology

• Primary apnea infant can be manually stimulated
  to start breathing again
• Secondary apnea requires resuscitation to
  reestablish respirationlasts for more than 30
  seconds as is associated with desaturation,
  bradycardia, and hypotension

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Asphyxia/Apnea

• Consequences
• Anoxic brain injury leading to necrosis of
  neurons and/or hemorrhage
• Periventricular leukomalacia brain infarct
• Other organ systems (heart, kidneys, GI tract)
  also suffer from ischemia
• Can lead to DIC
• In the lung, increases PVR and decreases
  surfactant production

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Apnea - Treatment

• Monitoring and treatment of ineffective
  respiration before it degenerates to apnea
• Low FiO2 oxygen may reduce apnea episodes
• Caffeine, theophylline, or doxapram can be used
  to stimulate respiration
• Oscillating bed

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Meconium Aspiration

• Meconium is the green-tinged bowel content of an
  infant which is usually passed within 48 hours
  after delivery
• Composed of swallowed amniotic fluid, salts,
  mucus, bile, cellular debris
• If the infant passes meconium into the amniotic
  fluid in utero, it may cause airway obstruction,
  air trapping, and bacterial growth
• Rarely occurs in infants lt36 weeks

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Meconium - Etiology

• Fetal passage of meconium occurs with
  intrauterine stress or hypoxia
• Hypoxia causes a vagal response that relaxes the
  anal sphincter allowing meconium to pass into
  amniotic fluid
• Normally, small amounts of amniotic fluid (up to
  5 ml) move into and out of the upper
  airwayshypoxia increases the risk of aspiration
  because of gasping respirations in
  uteroaspiration can also occur at birth
• Can cause a ball-valve effect in the
  airwaysdilation during inspiration allows air
  past the meconium which then becomes trapped on
  expiration causing hyperinflation and
  predisposing to air leaks
• The airways also become inflamed and secretion
  production increases
• Meconium may also hinder surfactant leading to
  atelectasis

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Meconium Clinical Presentation

• Usually a term or post-term infant covered with
  meconium at birth
• History may include prolonged labor, breech
  delivery, late decelerations
• Signs of resp distress develop quickly
  cyanosis, gasping respirations, grunting,
  retractions, flaring, tachypneathe thicker the
  meconium the more severe the respiratory symptoms
• AP chest diameter is often increased
• Diagnosis is made at birth when the meconium is
  seen

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Meconium - Treatment

• To prevent aspiration into the lungs, pharyngeal
  suction should be performed when the head is
  delivered and before delivery of the thorax
  (before the first breath is taken)
• After birth, use the ETT as a suction catheter
  b/c suction catheters are too small and become
  clogged
• Surfactant replacement since meconium hinders
  surfactant
• Liquid ventilation meconium can float to the
  top and be removed

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Barotrauma

• Pneumothorax
• Most common type of barotrauma seen in babies
• Signs/symptoms
• Increased distress with retractions
• Tachypnea
• Bradycardia
• Cyanosis
• Hypotension
• Apnea
• Asymmetrical chest movement
• Absent breath sounds on affected side

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Pneumothorax

• Diagnosis
• CXR
• Transillumination
• Because skin is so thin, can place a light
  against the area of suspected pneumo and the
  light will spread out highlighting the pneumoyou
  get a uniform circle of light if theres no
  pneumo
• Treatment
• Chest tube/needle aspiration
• If its small and not causing any problems, it
  may be left alone to spontaneously absorb

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Other Barotraumas

• Pneumomediastinum
• Air is in the mediastinum
• Can compress SVC and IVC and affect blood return
  to the heart
• Pneumopericardium
• Air in pericardial sac around the heart
• Can cause a tamponade effect and drop CO
• Needle aspiration

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PIE

• Pulmonary interstitial emphysema
• Air is in the interstitial space around the
  alveoli
• Associated with high PIP, PEEP, and long It
• Can progress to pneumothorax/ mediastinum/pericard
  ium
• Best treated by prevention use as low a PIP as
  possible
• HFV has been used as well
• Putting baby on 100 oxygen has been done to
  create a nitrogen gradient and reabsorb the air

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Persistent Pulmonary Hypertension of the Newborn

• Characterized by increased PVR and occurs most
  often in infants who are term or postterm
• Associated with MAS, RDS, and birth asphyxia but
  can also be idiopathic
• Persistent right-to-left shunts (PDA, FO)

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PPHN - Etiology

• At birth, when the umbilical cord is cut, the
  lungs make the transition to becoming the organ
  for gas exchange
• PVR decreases because
• PaO2 increases
• pH increases
• Air expands the lungs
• Release of vasoactive substances, such as
  prostaglandins, bradykinin, and endothelium-
  derived relaxing factor
• In infants with PPHN, the decrease in PVR either
  fails to occur or is reversed by pulmonary
  vascular hyperreactivity to irritating stimuli

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PPHN Clinical Presentation

• Cyanosis, tachypnea, and hypoxia appear in first
  12 hours of life with signs of respiratory
  distress
• Hypocalcemia and hypoglycemia may develop rapidly

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PPHN - Diagnosis

• Hyperoxia test PO2 is evaluated on room air and
  then after 100 for 20 minlittle to no change
  indicates a R-to-L shunt which may be PPHN or
  congenital heart disease
• Preductal-Postductal PO2 right radial PO2 is
  compared with umbilical or transcutaneous
  measurements from the upper chest are compared to
  the abdomenR-to-L shunt is present if theres
  gt20 mm Hg differencecan also occur with
  congenital heart defects
• Hyperoxia-hyperventilation test infant is
  hyperventilated to a PCO2 of 25PPHN is present
  if PO2 increases gt100 mm Hg
• Doppler/Cardiac Cath show the shunts through
  the ductus arteriosus and foramen ovale

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PPHN - Treatment

• Oxygen high FiO2 to vasodilate pulm vessels
• Mech Vent hyperventilation to 25 mm Hg b/c resp
  alkalosis reduces PVR
• Infusion of tolazoline to dilate pulm vessels and
  reduce PVR
• NO reduces PVR