A case of preterm with severe RDS with PPHN with neonatal sepsis

1. A case of Preterm with RDS with
PPHN
Presented by Dr Gururaja R
MD, DNB (Paed)

2. Why this case presentation?
• Female neonate, Extreme
preterm (29wks)
• Very low birth weight(1.3kg)
• Severe respiratory distress
syndrome
• Severe persistent
pulmonary hypertension
• Severe hypoxemic
respiratory failure
• A NIGHT MARE FOR ANY
PAEDIATRICIAN

6. Present case – antenatal background
• Born to 27 yr old multipara (P3L2) mother
• Mother had prolonged PPROM (>4 weeks)
and chorioamnionitis – Significant risk factors
for neonatal sepsis and neonatal chronic lung
disease
• Mother received adequate antenatal steroids

7. Present case - Events in first hour of
birth
• Did not cry immediately
after birth
• Resuscitation done
• Endotracheal intubation
due to poor spontaneous
respiratoy efforts
• Mechanical ventilation
• Chest x ray features
suggestive of Severe RDS

8. Present case - Events in first hour of
birth
• Surfactant administration
• Second line antibiotics
• (piperacillin-tazobactum
and amikacin) in view of
risk factor of maternal
chorioamnionitis
• Mechanical ventilation
continued
• Central line
• TPN

9. Present case – subsequent events
• No improvement in oxygenation
• Required 2 and 3 dose of surfactant
• Required High frequency ventilation(HFOV)
due to failure of conventional ventilation
• Showed features of severe PPHN (persistent
pulmonary hypertension of new born)
requiring inhaled nitric oxide (iNO) along with
HFOV

10. Normal Post natal transition
• Umbilical Cord is
clamped and cut
• Placental supply is
removed
• Baby starts crying
• Lungs expand
• Drop in pulmonary
vascular resistance
• Increase in systemic
resistance

12. What happens in Respiratory distress
syndrome of preterm neonates?

13. Persistent pulmonary hypertension
(PPHN)
• This neonate developed PPHN
because of maladaptation --- reflex
vasoconstrction of pulmonary
vasculature due to hypoxia
• Cause - RDS
• Significant difference between
preductal and postductal SpO2
(>10%)
• Oxygenation Index >20
• Bedside echo – TR, PDA

14. PPHN - etiology

15. Three
pathways for PPHN

16. When to suspect PPHN?
• Severe hypoxia disproportionate to chest x-ray
• Labile or fluctuating oxygenation
• Heart murmur (TR, PDA)
• ABG – hypoxia and normal CO2
• Post ductal saturation > 10% difference compared
to preductal

17. How to confirm PPHN?
• Pre and post ductal saturations
• Echocardiography – TR, PDA
• Septal bulge to left
• Dilated RA and RV

18. Echocardiographic features of PPHN

19. How to assess severity of PPHN?
• Oxygenation index
• MAP X FiO2/PaO2 X 100
• Mild - <15
• Moderate – 15 to 25
• Severe - 25 – 40
• Very severe > 40
• Oxygen saturation index ?

20. Management steps
• 1. reverse reflex vasoconstriction
• 2. recruit alveoli
• 3. select pulmonary vasodilators

21. What was done in this case to tackle
PPHN?
• Thermo neutral environment
• Minimizing unnecessary handling
• Sedation , analgesia
• Fluid balance maintenance
• Glucose and calcium homeostasis

22. What was done in this case to tackle
PPHN?
• Mechanical ventilation
• Inhaled nitric oxide therapy
• Inotropes to keep systemic vascular pressure higher
than pulmonary vasculature pressure and optimal
tissue perfusion
• Antibiotics for neonatal sepsis
• Correction of anemia

23. Rescue High Frequency ventilation to
recruit alveoli

24. Inhaled nitric oxide therapy
for pulmonary vasodilatation
• Frequently used with
HFOV
• Increases cyclic GMP
resulting in pulmonary
vasodilatation

26. Subsequent course
• The neonate responded well and weaned off from inhaled nitric
oxide therapy
• Switched back to conventional ventilation from high frequency
ventilation
• Minimal enteral nutrition started
• How ever sepsis was still persistent
• Antibiotics upgraded to third line to cover gram positive , gram
negative and fungal organisms (meropenem, vancomycin,
tigecycline and caspofungin)

27. D1 vs D4

28. Subsequent course
• Situation appeared better on day 5
• Inotropes stopped
• Enteral nutrition started
• Extubated on day 7
• “Then came the shocker”?

29. Subsequent course
• Day 7, baby noticed to have severe pallor, bulging anterior fontanelle
• Thrombocytopenia (52,000)
• PBS showed evidence of sepsis
• Transcranial USG showed intraventricular haemorrhage with extension to
surrounding brain tissue (grade 4)
• There was bleeding from GIT and lungs evidenced by blood in ET tube
• Severe Neonatal Sepsis with DIC with grade 4 Intra ventricular
haemorhage
• Platelet transfusion followed by PRBC and FFP transfusions

30. What happened to this neonate at this
stage? Why IVH?
• Sepsis --- activation of coaugaltion system
with platelet consumption and fibrinolysis ---
DIC
• Multiple bleeding sites - lung, brain, GIT
• Grade 4 IVH

31. Intraventricular haemorrhage in
preterms

34. Subsequent events
• The neonate progressively deteriorated and
had respiratory failure requiring mechanical
ventilation
• She had cardiac arrest at 15:15 hours on 01
May 2022 and could not revived despite
resuscitation
• Declared dead at 1600 hrs on 01 May 2022

35. Where we went wrong? – lessons
learnt
• Premature (29 wk) low birth neonate (1.3 kg) born to a mother with
severe oligohydramnios with PPROM for more than 4 weeks with
chorioamnionitis
• Severe RDS with PPHN and hypoxemic respiratory failure and later
developed severe neonatal sepsis with DIC
• Prematurity is a non modifiable risk factor
• Immature lung, brain, gut and immune system
• Adequately managed for initial RDS, respiratory failure and PPHN
• We lost the baby due to severe neonatal sepsis and its complications
• Immature immune system poses the preterm at a higher risk factor for
sepsis – non modifiable
• Any preterm neonate with tubes in so many places at risk for health care
associated infections - modifiable
• Health care associated infections can be prevented with adequate bundle
care approach and team effort

36. •THANK YOU