Print Page   |   Contact Us   |   Sign In   |   Register
Guide to Neonatal Ventilation Case Study 5

Back to Main Menu


Ventilation Management of MAS, PPHN, and Air Leaks
Meconium aspiration syndrome is one of the most common causes of severe respiratory failure in infants born at term/post-term gestation. Inhalation of meconium causes airway obstruction, atelectasis, epithelial injury, surfactant inhibition, and pulmonary hypertension, the chief clinical manifestations of which are hypoxemia and poor lung compliance.
  • Prenatal History: Baby B was born via emergency cesarean section at 39 6/7 weeks gestation to a 39-year-old Caucasian mother G5, P4, who presented late to care. Her first prenatal visit was at 39 3/7 weeks secondary to headaches and dizziness. She had a history of chronic hypertension and was diagnosed with preeclampsia and placental insufficiency; the fetus with intrauterine growth restriction. Induction of labor failed and a cesarean section was performed. Maternal laboratory studies were all normal. The mother’s blood type was O positive, Coombs (direct antiglobulin test [DAT]) negative.
    Apgar scores were 1, 4, and 7 at 1, 5, and 10 minutes respectively. The infant was covered in meconium. He cried initially after birth, then was apneic and floppy, needing suction, positive pressure ventilation (PPV), and oxygen. He recovered initially and was sent to the postpartum floor with his mother.

  • Questions
    1. What are the risk factors for MAS?
    2. What is the pathophysiology of MAS? 

  Day of life (DOL) 0-3  

  • At 90 minutes of age the infant developed the following signs: Tachypnea, intercostal retractions, coarse bronchial sounds, expiratory grunting, and poor color. He was admitted to the NICU for ongoing care. His chest appeared barrel-shaped. A chest x-ray (CXR) revealed bilateral patchy areas of increased density and flat diaphragms (Figure 1).
    He was initially placed on continuous positive airway pressure (CPAP), but after a series of worsening blood gases was intubated and placed on high frequency oscillatory ventilation (HFOV) with the following settings: Amplitude: 26, mean airway pressure (Paw): 14 cm H2O, Hz: 9, IT: 33 %, FIO2 0.50–0.08. On exam after transition to HFOV the infant displayed chest bounce to the abdomen and breath sounds were equal on auscultation. HFOV was choosen in this case because of refractory hypoxemia and presumed gas trapping, evidenced by blood gas findings and hyperexpansion noted on x-ray.
    The following ventilation challenges existed for this infant: non homogeneous lung disease; regions of hyperinflation; surfactant inactivation; atelectasis, leading to ventilation perfusion mismatch and hypoxemia; worsening acidosis and hypoxemia; very dynamic changes in lung compliance; and pulmonary vasoconstriction placing the infant at risk for PPHN.
    An arterial blood gas (ABG) done after one hour on HFOV was: pH 7.25, PCO2 55 mm Hg, PO2 53 mm Hg, HCO3 19 mEq/L, Base Excess (BE): -5. At six hours of age, Baby B developed a pneumomediastinum (Figure 2), and was placed on high frequency jet ventilation (HFJV) with the following settings: PIP: 24 cm H2O, PEEP: 9 cm H2O, Rate: 360 bpm, no back up rate, FiO2 0.40–0.60.
    Arterial blood gas results after 30 minutes on HFJV were as follows: pH: 7.26, PCO2: 62 mm Hg, PO2: 65 mm Hg, HCO3: 19 mEq/L, BE: -6. The HFJV settings were changed to PIP 26 cm H2O , PEEP 10 cm H2O. A repeat ABG was drawn one hour later with the following results: pH: 7.32, PCO2: 52 mm Hg, PO2: 61 mm Hg, HCO3: 21 mEq/L, BE: -3. 
  •  Questions
  1. What are the common radiologic findings associated with MAS?
  2. What are the treatment strategies for the clinical management of MAS?
  3. What is the pathophysiology of the pneumomediastinum?
  4. What are the basic principles of and differences between HFOV and HFJV?
  5. How is the PCO2 affected by changing the settings on the HFJV?

 

DOL 4-5

  • The infant was placed on HFJV but did develop bilateral pneumothoraces (Figure 3). Both were needle aspirated.

  • Questions
  1. What factors in this infant’s history put him at risk for air leak?
  2. What are the air leaks that can be seen on chest x-ray?
  • For more information to answer these questions refer to the following learning resources.
    • Review of Air Leaks
      Air Leak Syndromes. Excerpted from Acute Respiratory Care of the Neonate.(3rd ed., pp. 195-198).


DOL 6

  • The infant had a reaccumulation of air in the area of the left pneumothorax, with accompanying clinical deterioration. He developed a 10–15 point pre- to postductal saturation difference and he was poorly oxygenated despite adequate blood pressure. His ABG at this time was: pH: 7.12, PCO2: 50 mm Hg, PO2: 39 mm Hg, HCO3: 17 mEq/L, BE: -9.
    A cardiac echocardiogram was performed and persistent pulmonary hypertension of the newborn (PPHN) was diagnosed. Inhaled nitric oxide (iNO) was initiated at 20 ppm with a favorable effect and an increase in oxygen saturation levels.

  •  Questions
    1. What are the cardiac echocardiogram findings in an infant with PPHN? 
    2. What are the risk factors for PPHN?
    3. What are the ventilation strategies for an infant with PPHN?
    4. What changes take place during the normal transition from fetal to neonatal circulation?
    5. What is the mode of action of iNO?
    6. What is the half-life of iNO and what implications does this have for practice?
  •  For more information to answer these questions refer to the following learning resources.
    • Review of PPHN and iNO
      Persistent Pulmonary Hypertension of the Neonate. Excerpted from Acute Respiratory Care of the Neonate.(3rd ed., pp. 42-47).
      Pulmonary Hypertension in the Neonate—14th National Advanced Practice Neonatal Nurses Conference, April 2017.
      Transitional Events. Excerpted from Acute Respiratory Care of the Neonate.(3rd ed., pp. 13-16).


  • Available CEU's (processing fees required)

  • About the Contributor

    Julieanne Schiefelbein, DNP, M AppSc, MA(Ed), CNM, CPNP, NNP-BC, NPT-BC, received her initial Masters degree from the University of Sydney, while she worked as a clinical nurse specialist prior to moving to the U.S. to become a neonatal nurse practitioner. She received her Neonatal Practitioner qualification from Georgetown University, and her Pediatric Nurse Practitioner qualification, and Doctor of Nursing Practice from the University of Utah. She currently works for Intermountain Health Care in Salt Lake City, Utah, as a neonatal nurse practitioner. She also teaches in the NNP track of the DNP program at the University of Utah. Julieanne served on ANN's Executive Committee from 2014 to 2016.

     

    Community Search
    Sign In