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PPHN in a premature infant with RDS, GBS sepsis and born after placental abruptio


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Hi colleagues,

I had the pleasure recently to manage a premature infant (30wks EGA), who was born by precipitously vaginal delivery after mother arriving at the hospital with abdominal pain and vaginal bleeding, (later confirmed to be placental abruption). Good prenatal care, GBS positive in mother's urine 3wks PTD. The female infant was born lifeless, required PPV and chest compression by the bedside nurse  and was intubated quickly when the neonatology arrived at the bedside at 2 MOL. Apgars 1,3 and 7. Infant was brought to the NICU placed on CMV initially at 20/5, then increased to 25/5, RR of 40, FiO2 40-60%; suvanta given and PIP pressures reduced slowly to 18/5. BP unreadable, very poor perfusion noted. BW 1.2kg.. UAC.UVC placed. Initial ABG 7.1/58/-12.5(not too bad). Infant had received 2NS boluses by the time I arrived. BP still with a mean in the low twenties and very poor skin perfusion at this point. Abx ordered and given stat. Initial Hct of 32%. PRBC ordered and given within 2HOL. After PRBC color improved and FiO2 was 30%, although BP was still low and a repeat ABG 7.2/53/PaO2 49/-5.1. Initial BS was also low and three glucose boluses given and GIR adjusted. Hydrocortisone one dose was given.  An ECHO was ordered at this point and severe PPHN with suprasytemic pulmonary pressures was noted, normal cardiac function otherwise, large PDA bidirectional shunt. Infant was started on Dopamine at 10mcg/kg/min with titration to maintain systolic BP >50, up to 15mcg and dobutamine later added at 5 mcg with good response. PEEP was increased to 6 and FiO2 was increased to achieve a PaO2 in the 80 to 100.

At this point, a blood culture was reposted positive for gram positive cocci in chain (later reported as GBS). Once BP was stable, fentanyl and versed were started PRN to keep the infant sedated and comfortable. A dose a NaBicarb was given later on with a -7.5  base deficit, which was infused over 2hrs(acidosis was felt to be related to urinary bicarb loss) and a Calcium run for a iCa of 0.8. Infant slowly improved and is now on 2 LPM of HHFNC at 21%, off vasopressors, repeat ECHO with no PPHN.

Question:

1- Did this infant truly have PPHN? it is not uncommon to see mild transient elevated right ventricular pressures in premature infants with RDS, but this infant was clinically unstable and had three factors that could lead to malignant PPHN if untreated. I do understand the limitation of echocardiography in the diagnosis of PPNH, but given the risk factors and clinical presentation I felt and could not wait and see what happens. I would love to hear your personal experience in this type of patients in regard to diagnosis.

2- How different from the term infant do you manage premature infant with significant PPNH? I was trained to manage then equally, except for INO and <34wks, but I will still address the factors that aggravate PPHN such as hypoxemia, anemia, hypotension, hypoventilation, hypothermia, acidosis, agitation and hypocalcemia.

2- What is your experience with the use of sedation, paralysis in premature infant with PPHN? my practiced have been to avoid pain and agitation with PRN doses of fentanyl or Morphine and a benzodiazepine. I do not routinely use a fentanyl or verses drip or paralysis in my preemies with PPHN.

3- What about bicarb in PPHN?: Over the past few years, there have been a significant criticism to the use of bicarb in the NICU particularly in the acute setting with acidosis, but in the infant with PPHN, I still use it, particularly when I have achieve good perfusion, adequate ventilation and acidosis persists. My practice in this situation is to infuse bicarb very slowly  over 2-4hrs and next day add acetate to the TPN

Thanks for sharing your personal opinions in this topic

best wishes

respectfully

Dr. Guerra

 

 

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