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Respiratory Distress in The Newb

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					Respiratory Distress in the Newborn:
    Recognition and Treatment
        WADAH KHRIESAT,MD
             Respiratory Distress
• Hyaline Membrane Disease- major cause
  – Pathophysiology
  – Surfactant and ventilator therapy
Must distinguish from other causes:
• Transient Tachypnea of the Newborn
• Pneumonia/sepsis
     Evaluation of respiratory distress
•   H+P
•   CXR
•   Hematocrit
•   Blood Glucose
•   Blood pressure
•   Blood gas status
   Clinical Features aid in diagnosis
• Gestational age
• Historical risk factors for infection
• Type of distress- grunting,flaring, retractions,
  tachypnea
• Associated anomalies
• Radiographs
Transient Tachypnea of the Newborn
• Mild and self-limited
• Increased RR, no retractions, mild cyanosis
• FiO2 < 0.4
• Usually term infants, C/S and maternal IV fluids
  associated
• CXR with prominent vascular markings
Transient Tachypnea of the Newborn
• Delayed resorption of fetal lung fluid

• Must consider, and rule out pneumonia
• Treat with antibiotics if diagnosis is uncertain
  – Oxygen need beyond six hours
  – Oxygen need increasing
  – Worsening symptoms           6
    Meconium aspiration syndrome
• MSF in 10-15% of births
• Rare before 34 weeks gestation
• More likely with thick staining or particulate MSF
• Thin staining in vigorous infant requires no
  special Rx
• Can’t prevent all MAS
           Meconium Aspiration
• CXR- increased density, irregular infiltrates
  – areas of hyper-expansion, areas of collapse
  – Fluffy non-homogeneous infiltrates
• May be hard to distinguish from retained fluid,
  pneumonia
       Neonatal Respiratory Disease
• Not every infant with respiratory symptoms has
  respiratory disease
• Consider Extra-pulmonary causes:
  –   Heart disease
  –   Hypovolemia, polycythemia, anemia
  –   Acidosis, hypoglycemia, hypothermia
  –   CNS hemorrhage, drugs, muscle disease
   Hyaline Membrane Disease(HMD)

• Once the major cause of mortality in premature
  infants
• Progress in treatment mirrors advances in
  neonatal medicine
• Effective treatment has improved survival at
  gestational ages as low as 24 weeks
         HMD - Clinical features
• Disorder of premature infants
• Respiratory distress
  – tachypnea, grunting,flaring, retractions
• Difficult to distinguish from pneumonia
• Severity peaks at 24-48 hours, resolution by 72-96
  hours (without surfactant therapy)
• Recovery prolonged by barotrauma or oxidative
  injury
       HMD - Pathologic features
• Characteristic injury to terminal airways
  beginning within the first few breaths
• Lungs are solid, congested, with destruction of
  epithelium of terminal conducting airways
• Hyaline membranes: coagulum of sloughed cells
  and exudate,plastered against epithelial basement
  membrane
          HMD- Pathophysiology
• Instability of terminal airspaces due to elevated
  surface forces at liquid-gas interfaces
• Stable alveolar volume depends on a balance
  between: 1)surface tension at the liquid-gas
  interface, and 2) recoil of tissue elasticity
         HMD - Pathophysiology
• Terminal airspaces are not uniform throughout the
  lung
• There is a range of critical opening and critical
  closing pressures in various alveoli
• Some alveoli remain collapsed, some are
  ventilated but collapse during expiration, and
  some remain ventilated during inspiration and
  expiration (the goal)
         Lung Function in HMD
• Reduction in FRC from 30 ml/kg, to as low as 4-5
  ml/kg. Caused by loss of volume and interstitial
  edema.
• FRC mirrors changes in oxygenation.
  Improvements can be due to distending pressure,
  surfactant replacement, or clinical resolution
           Lung Function in HMD
• Lung Compliance is also reduced: from 1-2 to 0.2 -0.5
  ml/cmH2O-kg
• Reduction due to decreased number of ventilated alveoli,
  and increase in recoil pressure of ventilated airspaces

• Lung resistance is significantly increased
• Usually, impairment in ventilation is less pronounced
  than altered oxygenation
                 Initial Care
• Maintain warmth- cold stress will mimic other
  causes of distress
• Monitor blood glucose levels- assure they are
  normal
• Provide enough oxygen to keep the baby pink
           Temperature Control
• Body Temperature that is too high or too low will
  increase metabolic demands
• When oxygen uptake is further compromised by
  disease, increased demand can not be met
• Servo controlled warmers are very helpful, but
  can be mimicked by frequent assessment
           Temperature Control

First things first:
• Dry the baby
• Keep the baby warm
• Use shields to decrease evaporative and
  convective losses
• PUT A HAT ON THE BABY!
                  Initial Care
Ensure adequate hydration:
• Start fluids at 70-80 ml/kg/d 10% glucose
  solution
• Smaller babies may need more fluid
• Add electrolytes by the second day

• On day 3-4 watch for diuresis
               Assess circulation
•   Monitor heart rate
•   Assess Blood pressure
•   Check peripheral perfusion and capillary refill
•   Avoid excessive blood sampling
                   Initial Care
Consider other etiologies:
• INFECTION,INFECTION
  – Evaluate
  – Begin antibiotic therapy as prophylaxis
  – Continue as clinically indicated
• Anatomic malformations
                  Clinical features
• Risk factors:
  – Prematurity
  – maternal diabetes, maternal bleeding, perinatal
    asphyxia, C-section without labor
  – White race, male sex
• Features :
  – Early onset, from birth to four hours
  – uncomplicated clinical course with progressive
    worsening until day 2-3 and onset of recovery by 72
    hours
          Clinical features (contd)
• Physical Examination
  – Brief but thorough
  – Signs of respiratory distress :
     •   Cyanosis
     •   Tachypnea ( >60/min, shallow, rapid )
     •   Grunting ( delayed expiration maintains FRC )
     •   Retraction ( Subcostal, substernal, intercostal )
     •   Flaring ( 50% airway resist in nose& pharynx)
  – Temperature, Blood pressure, Skin perfusion
              Management
• Concepts
  – Respiratory
     • Prevent hypoxia and acidosis
     • Prevent worsening atelectasis, edema
     • Minimize barotrauma and hyperoxia
  – Supportive management
     • Optimize fluid and nutrition management
     • Perfusion, Infection, Temperature control
    Surfactant replacement therapy
• When: Prophylaxis (prevention) vs.
  Treatment (rescue) ; Early vs. Late
• What: Synthetic preparation (Exosurf) vs.
  Mixed Natural/Synthetic (Survanta)
• How: Administration : Indications, Dosage,
  Technique
• Additives : Antioxidants
    Surfactant replacement therapy
• Prophylaxis vs Rescue
  – Four major trials so far ( Dunn et al, Kendig et al,
    Merritt et al, Egberts et al )
  – No significant difference in mortality, BPD.
    Possible minor decrease in pneumothorax with
    prophylaxis
  – Prophylaxis leads to overtreatment, logistics
    difficult - immediate manipulation in delivery room
    Surfactant replacement therapy
• Early treatment vs. delayed selective treatment
  – The OSIRIS Collaborative Group 1992
  – Early (<2hrs age) vs delayed selective treatment
    :6774 babies, international
  – Early treatment led to a small, but significant
    reduction in risk of death or O2 dependence at
    term-adjusted age (RR 0.84)
      Surfactant replacement therapy
• Dosage: Survanta 4cc/kg (Max 8cc) q 6-12
           ( 100mg/kg phospholipids )
• Administer through side-port ETT adapter, do not need
  to remove from vent or pass catheter
• Three doses better than one dose
  ( American Exosurf Neonatal Study )
• Two doses as good as 3-4 doses ( OSIRIS)
• Minimum two doses; if sick, may give up to 4.
• Retreatment criteria open to question
     Surfactant replacement therapy
• Unclear if positioning is required during
  administration
• Commonest side effects are transient bradycardia
  and desaturation
• Rare association with pulmonary hemorrhage (
  temporal association with PDA )
• Rapid improvement in PO2 due to better V/Q
  matching, slower improvement in PCO2 and
  compliance.
                       CPAP
• Indication: Significant respiratory distress, FiO2 >
  0.40
• Start with Nasal prong CPAP, 5 cm H2O pressure,
  flow 5-10 lpm, FiO2 0.40-0.60
• Increase pressure in steps of 1-2 cm H2O till 8-9
  depending on resp effort and PO2.
• Wean by decreasing FiO2 in steps of 0.05 till 0.40,
  then wean CPAP in steps of 1-2 cm H2O till 4-5,
  then discontinue.
                     CPAP
• Concept:
  – Prevents atelectasis
  – reduces pulmonary edema
  – shifts infant to breathe on more compliant portion
    of pressure volume curve
• Problems:
  – High CPAP may decrease venous return
  – High CPAP may decrease minute ventilation
  – Abdominal distension, open mouth, crying
         Mechanical Ventilation
• Indications:
  – PCO2 >55 or rapidly increasing / pH<7.25
  – PO2 <50 with FiO2 >0.6-1.0
  – Severe apnea
• No role for elective intubation, whatever the
  birth weight
  – Babies grow just as well, whether on the ventilator
    or not.
  – Risks of intubation and barotrauma considerable.
    More ET / IMV=More BPD.
       Mechanical Ventilation
• Initial settings
  – PIP 20-25 , PEEP 4-5 cm H2O
  – Frequency 20-40/min
  – Ti 0.4-0.5 sec
  – Previously required FiO2 0.5-1.0
  – Manual ventilation with anesthesia bag and mask
    will give an idea of pressures required.
           Mechanical Ventilation
• Continuous flow, pressure-limited, time-cycled
  ventilator conventional
• Adjustments
   – PO2 50-80 mmHg
   – PCO2 45-55 mmHg
   – pH 7.25-7.40
   – Blood gases q4-6 or more frequently +         15-
     20 mins following vent changes
   – ET suctioning as required. Chest physiotherapy in
     acute RDS not required, may be associated with
     IVH.
         Mechanical Ventilation
• Weaning once infant improves
  – Lower PIP to 30 in steps of 2-4 cmH20
  – Next reduce FiO2 to 50-60% by decrements of 5%
  – Then reduce PIP to 20 and PEEP to 5 in steps of 1-2
  – Decrease FiO2 to 40%
  – Decrease rate to 10-15/min; then PIP to 15-18, FiO2 to
    30%
  – Extubate tiny premies to NCPAP. May try larger babies
    on ETCPAP.
             Acute Complications
• Air Leak Syndromes
  – Consider with sudden change in condition
  – More common if baby receiving ventilatory support
  – Pneumothorax most common
• Therapy
  – None if stable
  – Oxygen 100%
  – Thorocentesis: Needle or tube
           Acute Complications
• Intracranial Hemorrhage
  – High risk if HMD is severe
  – More common at lower gestational ages
  – Rare above 33 weeks gestation
• Suspect if there is a sudden change in condition
• May coincide with development of air leak
• Signs: change in Fontanel, perfusion
              Acute Complications
• Patent Ductus arteriosus
   – Usually evident during resolution phase
• Signs of Congestive Heart Failure
   – Increased oxygen need
   – Cardiomegaly
   – Acidosis, decreased urine output
• Therapy:
   – Decrease fluid intake
   – Indomethacin

				
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posted:4/23/2010
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