Dr J P Soni

1. SHOCK IN NEONATE
Prof Jai Prakash Soni
Head of the Dep of Paediatrics
Division of Pediatric Cardiology
Dr S N Medical College
Jodhpur

2. Shock
Shock is an acute state in which circulatory function is inadequate to supply sufficient amounts of O2 and
other nutrients to tissues to meet metabolic demands.
Myocardial dysfunction, abnormal peripheral vaso-regulation and hypovolemia leading to decreased
delivery Of oxygen and nutrient to tissue are often primary source of neonatal shock.
This is often complicated by relative adrenal insufficiency in premature infant.
The neonatal myocardium has lower contractile elements as compared to children and adults
Immature myocardium has a higher basal contractile state
Higher sensitivity to change in afterload
Neonate have higher water content
Greater surface to volume ratio
Reliance on extracellular calcium store

3. The vascular smooth muscle tone and a complex regulation play a key role in pathogenesis of neonatal
shock.
A balance of the vasodilating and vasoconstricting forces regulates the tone commonly described factors
including vasopressin, nitric oxide, eicosanides, catecholamines and endothelin.
Pathophysiology of shock in newborns is unique since it is associated with physiologic transition from fetal
circulation to neonatal circulation at birth.
Supra-systemic pulmonary vascular resistance (PVR) in the prenatal period may remain elevated , especially
in the presence of ongoing hypoxia and acidosis from sepsis, leading to PPHN
There is plenty of evidence suggesting low cortisol level in sick term, late preterm and preterm infants.
Both adrenal insufficiency and decreased vascular responsiveness to catecholamine can contribute to
vasopressor or resistant shock. Low dose steroid have been found to improve cardiovascular status in
infant with vasopressor resistant shock.

5. Common clinical shock scenarios in neonates are
1. VLBW neonates during transitional circulation in first 24-48 hours of life
2. TERM BABY WITH MAS – PPHN
3. Hypoxic ischaemic Encephalopathy HIE – LV dysfunction
4. CHDs- critical CHDs
5. Baby with large PDA – Pulmonary hyper-perfusion and systemic hypoperfusion
6. Sepsis – distributive shock – due lossoc vascular tone
7. Volume Depleted States in neonate – dehydration shock
8. Post surgical

6. Shock
Hypo-Volumic Cardiogenic Hypo-volumic Obstructive
Peri. Eff
Pneumothorax
PPHN
Dissociated
Meth-
haemoglobinemia
Type of shock

7. List of the parameters used for assessment of neonatal shock
Conventional parameters Capillary refill time
Urine out put
Heart rate
Blood pressure
CVP
Lactic acidosis
Mixed venous saturation
Arterio- venous oxygen difference
New parameter ( in use) Functional echo-cardiography
Novel parameters (research) Functional cardiac MRI
Perfusion index

8. FUNCTIONAL ECHO- NEONATAL SHOCK

9. Shock
Cardiogenic
Impaired ability of heart to receive and pump blood to meet body demand

10. Following ECHO find in new born with MAS or in VLBW neonates
Enlarge RA and RV
Bulging of IAS and IVS on left side
TR
Right to left flow across PFO and PDA
Suggest High pulmonary pressure PPHN
or
Persistent fetal circulation in VLBW
Rx
NO
Milrinone
Sildenafil
MAS
High PAH

11. RV
RA
TR
TR
AO
PDA FLOW
PPHN PDA REVERSAL
RV
RA
RA
LA
LA
PFO
PA
TR
PDA REVERS FLOW PA TO AO

12. Following ECHO find in new born presenting as pulseless,
dusky in first few weeks of life
Enlarge RA and RV
Bulging of IAS and IVS on left side
TR
Right to left flow across PFO
Left to Right flow across PDA
Suggestive of Right side duct dependent lesion
Rx
Infusion of PGE1
Critical PS
With intact
IVS

13. Enlarge RA and RV small LV
Bulging of IAS and IVS on left side
MR
Left to Right across PFO
Right to Left across PDA
Suggestive of left side Duct dependent lesion
Rx
Infusion of PGE1
Critical AS
CoA
IAAS
Following ECHO find in new born presenting as pulseless,
dusky in first few weeks of life

14. Following ECHO find in new born
Enlarge LA and LV dysfunction
Bulging of IAS and IVS on RIGHT side
PFO flow from Left to Right
PDA flow from Right to Left
Suggest : Hypoxic LV dysfunction
Rx Inotrope infusion
Dobutamine
Milrinone
LV Enlarge
with
Poor EF

15. Following ECHO find in new born
Enlarge LV
Bulging of IAS and IVS on RIGHT side
PFO and PDA flow from Left to Right
Suggest : Parenchymal disease – Post surfactant and PEEP
Rx
oxygen with CPAP
LV enlarge
But
Good EF

16. Shock
Hypo-
volumic

17. Following ECHO find in new born presenting of 3-7th day of life with poor pulsation
Kissing IVC
IVC <8 mm with > 50% inspiration collapse
IVC >8 mm with no inspiration collapse suggestive of Hyper volumia
EF => 70 % suggestive of hypo - volumia
Rx
Fluid Infusion
10 ml / kg two to three bolus

18. Shock
Distributive

19. A 4 days 28 weeks Preterm neonate presenting with cold periphery, cyanosis & poor
pulsation,
Shock refractory to fluid infusion, inotropes and anti microbials
echo revealing
large PDA size > 2 mm
pulmonary hyper perfusion LA/AO = > 1.4:1
and
systemic hypoperfusion RI > 0.8 in ACA or MCA, DAO, CA and renal artery
and low SVC flow
shock may be due to large PDA ?

20. EVALUATION OF PDA
HAEMODYNAMICALLY SIGNIFICANT PDA -
YES /NO
PULMONARY HYPER PERFUSION LA/AO > 1.6, INCREASE PUL
VENOUS RETURN
LA/AO < 1.4
LA/AO >1.4

21. PDA CHARACTERISTICS DUCTAL SIZE > 2MM
PULSATILE PDA DOPPLER
NO PDA CONTRICTION
NON RESTRICTIVE L-> R Tiny PDA
PA
DAO
NON RESTRICTIVE L-> R Pulsatile PDA
PA
AO

22. PDA CHARACTERISTICS DUCTAL SIZE > 2MM
PULSATILE PDA DOPPLER
NO PDA CONTRICTION
NON RESTRICTIVE L-> R
BIDIRECTIONAL
RESTRICTIVE L-> R
Closing PDA
Tiny PDA
PDA reversal Right -> Left
PA
DAO
NON RESTRICTIVE L-> R
NON RESTRICTIVE L-> R
Pulsatile PDA

23. Flow pattern in
ACA
DAO
Celiac axis
Renal artery
Absent diastolic flow
suggestive of steal of systemic blood
because of PDA

24. Shock because of large PDA
Treatment include
1. Fluid restriction
2. Caffeine - It will take care of apnea as well as increase myocardial contraction,
increase left ventricular systolic function, renal perfusion and urine out put.

25. Following ECHO find in new born presenting of 3-7th day of life with Good pulsation
and Normal plethysmography
IVC >8 mm with < 50% inspiration collapse
EF => 45-65 % normal volumia
Rx
Infusion of Vaso-pressure –
Dopamine
Epinephrine
Nor – epinephrine
Both drugs can increase blood pressure in shock states, although norepinephrine is more
powerful. Dopamine can increase cardiac output more than norepinephrine, and in addition to the increase in
global blood flow, has the potential advantage of increasing renal and hepatosplanchnic blood flow.

26. No change in diameter of IVC during inspiration and expiration – suggestive of Hyper volumia
or cardiac tamponade

28. Inotropes like dopamine, dobutamine, epinephrine and norepinephrine are indicated via iv or io route
before central access is achieved when myocardial contractility remains poor despite adequate volume
replacement. Delay increases mortality 20-fold.
Dopamine is the first line drug although dobutamine raises systemic blood flow more effectively.
Doapmine has the potential advantage of increasing renal and hepato-splanchnic blood flow.
Dopamine shows preferential pulmonary vasoconstriction, which might be detrimental if, during the
management of infants with persistent fetal circulation.
Dopamine reduces TSH release making hypothyroidism diagnosis difficult.
Dopamine is converted into norepinephrine by the enzyme dopamine β-hydroxylase (DBH), with O2 and L-
ascorbic acid as cofactors.
Norepinephrine is converted into epinephrine by the enzyme phenyl-ethanolamine N-methyltransferase
(PNMT) with S-adenosyl-L-methionine as the cofactor.
Dobutamine does not have any effect on the α2‐adrenergic receptors. Dobutamine is preferred when
there is a need to improve low cardiac. Dopamine shows preferential pulmonary vasoconstriction, which
might be detrimental if it also occurs during the management of infants with persistent fetal circulation.

29. Epinephrine and norepinephrine raise mean arterial pressure.
Epinephrine is a potent inotrope and chronotrope, and a systemic (SAP) and pulmonary vaso-constrictor.
Epinephrine is more effective than dopamine at increasing cardiac output during hypoxia.
Epinephrine preserves the SAP/PAP ratio.
Epinephrine causes adverse hyperglycaemia requiring insulin, increased plasma lactate and inadequate
gastric mucosa perfusion.
Norepinephrine is indicated for “warm” shock in neonates
The best vasoactive drug schedule for premature transition shock is low dose dopamine and dobutamine,

30. Nitric Oxide is used in PPH (persistent pulmonary hypertension).
Triiodothyronine is an effective inotrope in newborns with thyroid insufficiency.
Phosphodiesterase inhibitors are used if cardiac output does not improve and high systemic vascular
resistance persists. Milrinone - an inodilator (inotrope/vasodilator) and selective phosphodiesterase type III
inhibitor improves myocardial contractility and relaxation by effects on calcium. It relaxes arterial and venous
smooth muscle. It is advocated in “cold shock” with high peripheral resistance. Limited data is available on use
of milrinone in preterm infants.
Arginine-vasopressin (AVP)30: Endogenous AVP, released in response to hypovolemia and hypotension, shows a
biphasic response in septic shock, with initial high levels followed by inappropriately low levels in later stages.
This justifies exogenous administration to correct hypotension in vasodilatory shock in children and also in
extremely-low-birth weight infants.
Terlipressin (TP) is a synthetic AVP analogue with prolonged action; it has higher affinity for vascular
receptors than vasopressin. It is an effective rescue treatment for refractory vasodilatory septic shock.31 It
is advocated as a last resort when septic patients remain hypotensive despite fluid resuscitation and high doses
of catecholamine.

31. Levosimendan (LS) - is an inodilator that has cardio-protective and anti-inflammatory effects2 . It is a
calciumsensitizing agent that acts by binding to myocardial troponin C, allowing more efficient contraction. In
peripheral vascular beds, LS causes vascular relaxation which reduces cardiac afterload and promotes coronary
vasodilation. LS’s potential utility is due to a number of reasons; it can be used with conventional inotropic
agents, it has a simple dosing regimen and does not worsen the diastolic dysfunction often present in structural
heart disease. Clinical experience confirms the potential beneficial effects of LS infusion in restoring
hemodynamics in infants with low cardiac output septic shock resistant to catechol-amines.
Granulocyte and granulocyte-macrophage colony stimulating factors (G-CSF, GM-CSF) increase the number of
circulating white cells but do not reduce mortality from neonatal sepsis or septic shock.34 Pentoxifylline is a
carbonic anhydrase inhibitor that improves white cell function. One RCT in prematures shows significantly
reduced multi-organ failure, mortality and coagulopathy with improved BP blood.
Intravenous immunoglobulin (IVIG): Polyclonal and IgM-enriched IVIG reduces mortality from sepsis in the
newborn. Tumour necrosis factor can be blocked by various antagonists. Generally immunomodulators have
shown frustrating results in newborn septic shock management.
Protein C. Low PC plasma activity correlates with adverse outcomes, such as multiple organ failure and
mortality. It is a useful predictor of organ failure in severe sepsis and an important factor of high diagnostic
and negative prognostic significance. It is successfully used in term neonates and preterms at high-risk of
haemorrhage with sepsis-induced coagulopathy.

32. A. Early detection Early recognition and intervention are crucial for favourable outcomes of SHOCK.
B. Aggressive fluid therapy
Mortality is significantly reduced if hemodynamic function is optimized early. There is no advantage in using
crystalloids instead of colloids in septic shock. Intraventricular haemorrhage and infection transmission is
lower with crystalloids. The incidence of pulmonary edema is less with 5% albumin. Bolus resuscitation as a
life-saving intervention in shock without hypotension is challenged. Infants who do not diurese after
adequate fluids may need diuretics to prevent fluid overload.
C. Antibiotics
Blood cultures, biochemical markers for sepsis, blood glucose and ionized calcium should be taken before
initiating antibiotics for suspected sepsis.19 Ampicillin plus gentamycin is more effective than cefotaxime plus
gentamycin. Cefotaxime is preferred for meningitis.
D. Respiratory support Respiratory failure accompanying shock requires elective ventilation. Anoxia and over-
distension of alveoli- a potent IL-6 inducer should be avoided

33. E. Metabolic support
There is no consensus on ideal blood sugar but it should not be lower than 30 mg/dL.21 Level of 175
mg/dL or more has a 2.5X increased mortality; same in ELBW babies with level above 150 mg/dL.
Insulin should be used only when sugar level exceeds 180mg/dL in refractory shock and unfavourable
response new-born. There is no evidence to support bicarbonate therapy in acidemia of septic shock.
Hypocalcaemia is a reversible cause of cardiac dysfunction; it should be normalized. Corticosteroids
often used in septic shock when volume expansion and inotropes are unable to raise BP, appear to
increase mortality in a subset of patients. Consequently, corticosteroids are recommended for
refractory shock when adrenal insufficiency is suspected.
F. Nutrition
In infants with poor muscle mass and energy reserves, metabolic requirements increase due to
hypercatabolic state in sepsis. Appropriate enteral feeding to reduce bacterial translocation from gut
mucosa and preserve gut mucosal function is advocated.