INTENSIVE CARE

Utilizing Inhaled Nitric Oxide Noninvasively
Following Extubation
Laura Lerch, BS, RRT-NPS; Michael A Porte, MD
Inhaled Nitric Oxide for the use of Meconium Aspiration
Syndrome with pulmonary hypertension (PPHN) is clinically
indicated and practiced nationally. Clinical objectives for
ventilating infants noninvasively are to reduce ventilator induced
lung injury (VILI), to reduce ventilator associated infections,
and to reduce sedation. We present a case of severe Meconium
Aspiration Syndrome, in a term infant who continued to require
inhaled nitric oxide, based on echocardiogram evidence of
persistent pulmonary hypertension (PPHN), after extubation.
The patient received iNO through a RAM cannula.
Introduction
Meconium is present in amniotic fluid in 10-15% of all deliveries.
Aspiration occurs in 2-6% of those. 1 The more depressed the baby
as reflected by Apgar scores and arterial cord blood metabolic
acidosis, the greater the likelihood of aspiration syndrome
(MAS). Of those with MAS, 30-60% require mechanical ventilation
and 2-7% will die. 2 Furthermore, greater than 20% of infants
with meconium aspiration syndrome have PPHN. Management
of MAS needs to be thoroughly investigated to help understand
what the optimal management should be. 2
Case Report
This is a case report about a 3.150 kg infant male, born at 40 and
4/7 weeks gestation. He is born via normal, spontaneous vaginal
delivery with an uncomplicated maternal history at an out-born
hospital. Delivery was complicated by thick meconium stained
amniotic fluid and a nuchal cord was present. Resuscitation
was preformed following Neonatal Resuscitation Program
guidelines. Intubation for meconium was completed twice.
Chest compressions were required for thirty seconds. Apgars
were 3 (at one minute of life), 5 (at 5 minutes of life), and 7
(at ten minutes of life). The infant remained intubated with
endotracheal tube CPAP (continuous positive airway pressure)
until the neonatal transport team arrived from our Level Three
facility.
per minute, inspiratory time .35 seconds, and 0.90 FiO2 (fraction
of inspired oxygen). Initial capillary blood gas revealed a
respiratory acidosis 7.19/pCO2 78 mmHg/ HCO3 29.7 mmol/L/-1.0
(base excess). Ventilator settings were increased to a peak
pressure of 22 cmH2O with a respiratory rate of 60. Transport
stabilization was completed, and infant was transported to a
Level Three NICU. Hypoglycemia was treated with boluses of
D10W.
On admission to the NICU, venous blood gases showed
worsening respiratory acidosis: 7.13/pCO2 84 mmHg/HCO3
26.7 mmol/L/-4.9 (base excess), despite increased ventilator
settings. Oxygen requirement was at 80%. Surfactant was
given once. Follow up VBG improved: 7.30/pCO2 49 mmHg/
HCO3 23.3 mmol/L/-3.2 (base excess). Oxygen requirements
remained at 70% to 80% to keep oxygen saturation greater than
94%. The infant had persistent tachypnea despite ventilator
change from SIMV to A/C (assist control) and the addition of
IV Morphine for sedation. A UVC was placed. A peripheral
arterial line was eventually inserted. An EEG started due to
perinatal cardiorespiratory depression and clinical observation
of ‘twitches’.
Upon arrival of the Transport Team, the infant was placed
on conventional ventilation with ventilator mode SIMV
(synchronized intermitted mandatory ventilation), a PIP
(Peak inspiratory pressure) of 20 cmH2O, PEEP (positive end
expiratory pressure) of 5 cmH2O, respiratory rate of 45 breaths
Laura Lerch is a Neonatal Clinical Specialist of Respiratory Care at
UnityPoint Health-Meriter Hospital, Madison, WI. Dr Michael Porte is a
Clinical Professor Pediatrics at the University of Wisconsin, division of
Neonatology, UnityPoint Health-Meriter Hospital, Madison, WI.
DOL 1: High endotracheal tube terminating at the thoracic inlet.
Recommend advancement by 5 mm. Findings compatible with meconium
aspiration. Probable tiny bilateral pleural effusions.
28 neonatal INTENSIVE CARE Vol. 29 No. 4 • Fall 2016