This document provides an overview of shock in neonates. It discusses the pathophysiology of various types of shock seen in newborns, including cardiogenic shock, pulmonary hypertension, right heart hypoplasia/single ventricle lesions, left heart obstructive lesions, and distributive shock. It describes the role of echocardiography in evaluating neonatal shock and outlines the management principles, including aggressive fluid resuscitation, antibiotics for suspected sepsis, respiratory support, metabolic support with glucose and calcium monitoring, nutrition, and inotropic support when needed. The document emphasizes the importance of early recognition and intervention in shock for improved outcomes in neonates.

1. SHOCK IN NEONATE
Dr j p soni

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 and 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 physiological 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.

4. Pulmonary Hypertension Cycle
In Utero
MAS
Perinatal asphyxia
CDH
PPHN
Neonatal
MAS
Asphyxia
Sepsis
RDS
Pneumonia
Pulmonary Vascular Bed
Birth Lung
Disease
Hypoxia
Respiratory
&
Metabolic
acidosis
Increased Vascular resistance
Right to left shunting
across PFO & PDA

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 – d TGA, Critical AS, HLHS, Critical PS
5. Baby with large PDA – Pulmonary hyper-perfusion and systemic hypoperfusion
6. Sepsis – distributive shock – due loss of vascular tone
7. Volume Depleted States in neonate – dehydration shock , neonate with APH
8. Post surgical

6. Shock
Hypo-Volumic Cardiogenic Septic
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. Shock
PAH
PPHN
Impaired ability of heart to receive and pump blood to meet body demand

11. A term new born with MAS or in VLBW neonates presented with
Cyanosis and poor peripheral pulsation. ECHO revealed
Enlarge RA and RV
Bulging of IAS and IVS on left side
TR
Right to left flow across PFO and PDA
Suggesting High pulmonary pressure PPHN
or
persistanat fetal circulation in VLBW
Rx
NO
Milrinone
Sildenafil
MAS
High PAH

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

13. Shock
RHHS
Impaired ability of heart to receive and pump blood to meet body demand

14. A new born presented with sudden onset pallorness and bluish
Discoloration and examination revealed weak pulseless,
Baby ECHO revealed
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

18. Shock
HLHS
Impaired ability of heart to receive and pump blood to meet body demand

19. Emergency ECHO revealed -
Enlarge RA and RV small LV
Bulging of IAS on right side 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
A new born came in emergency with sudden development of
Refusal to feed, RDS, paleness and cyanosis.
Examination revealed poor peripheral pulsation,

20. Flow from PA to DAO
H L H S

22. LA
LV
LV
RVRV
RA
LA
RA
CoA

23. Post-ductal CoA
Baby came at 15 days with Shock
Rx PGE1 stabilized and taken foe Balloon dilatation
Contributed by Dr V Arya

24. Before balloon dilatation AfterContributed by Dr V Arya

25. Shock
Admixture

26. AO PA
PAD
A new born came in emergency with sudden deveolpment of
Refusal to feed, RDS, deep cyanosis and examination
revealed poor peripheral pulsation,
Emergency ECHO revealed -
Bulging of IAS on left side and intact IVS
Right to left flow across small PFO
Right to Left flow across constricting PDA
With d TGA closing PDA
Suggestive of Duct dependent d TGA
Rx
Infusion of PGE1

28. Shock
LV
dysfunction

29. Emergency ECHO revealed
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
ECG : SVT
Suggest : Hypoxic LV dysfunction
Rx Inotrope infusion
Dobutamine
Milrinone
LV Enlarge
with
Poor EF
A new born came in NICU with birth asphyxia, RDS,
Develop poor peripheral pulsation, unrecordable BP on day third

30. Emergency ECG :
and ECHO revealed
Enlarge LA and LV dysfunction
Bulging of IAS and IVS on RIGHT side
PFO flow from Left to Right
PDA closed
Suggest : tachycardia induce LV dysfunction
Rx Adenosine bolus
LV Enlarge
with
Poor EF
A new born came in NICU with birth asphysia, RDS,
Develop poor peripheral pulsation, unrecordable BP on day third

32. Shock
Lung
parenchymal
disease

33. A 28 weeks preterm new born had RDS and X ray revealed HMD.
Baby was given surfactant and put on CPAP –oxygen
Post surfactant baby was oxygen dependent and Emergency ECHO
Revealed
Enlarge LV
Bulging of IAS and IVS on RIGHT side
PFO and PDA flow from Left to Right
Suggest : parenchymal disease
Rx
oxygen with CPAP
LV enlarge
But
Good EF

34. Shock
Hypo-
volumic

35. new born presenting of 3-7th day of life with poor pulsation and ECHO revealed -
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

36. Shock
Distributive

37. A 4 days 28 weeks Preterm neonate presenting with cold periphery, cyanosis &
relatively Good 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 ?

38. Conical PDA
Window PDA
Tubular PDA
Aneurysmal PDA
Elongated PDA
Krichenko Angio-graphic type of PDA
1 st step -
Ductal characteristic &
Size

39. EVALUATION FOR
PULMONARY HYPER-PERFUSION
PULMONARY HYPER PERFUSION LA/AO > 1.6, INCREASE PUL
VENOUS RETURN
LA/AO < 1.4
LA/AO >1.4

40. PDA size 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
2ND STEP - PULMONARY HYPER-PERFUSION

41. PDA FLOW 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

42. Flow pattern in
ACA
DAO
Celiac axis
Renal artery
Absent diastolic flow
suggestive of steal of systemic blood
because of PDA
3RD STEP
SYSTEMIC HYPO-PERFUSION

43. SYSTEMIC HYPOPERFUSION RETRO GRADE FLOW IN -
DESCENDING AORTA absent diastolic or reverse flow
CELIAC AXIS OR SMA absent diastolic flow or reverse flow
MCA - absent diastolic flow or reverse flow
RETROGRADE FLOW IN DAO
RETROGRADE FLOW IN CELIAC AXIS

44. 4TH STEP - HEART ADAPTATION
Systolic function
FS Normal values – Term babies 25-41%
Preterm 23-40%
EF 45-55%
mVCF 1.5+ 0.04 cir/sec
SVC flow 62.5±20.93 Ml/Kg/min
Diastolic function
E/A Term baby >0.7: 1 , Preterm >0.6: 1
E/E’ <8 and suggests a normal left atrial pressure.
While values between 8 and 12 are
indeterminate, a value >12 is indicative of an
elevated left atrial pressure or PCWP
(>18mmHg).

45. 5TH STEP - SYSTEMIC
INVOLVEMENT
Find out Premature lung status
Find out - Brain - ICH - CRUSG
Gut - NEC – Clinical and X ray abdomen
Renal - Renal function- for failure - urine out put and
BUN

46. 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.

47. 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.

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

49. MANAGEMENT OF SHOCK

50. 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

51. E. Metabolic support
There is no consensus on ideal blood sugar but it should not be lower than 30 mg/dL. Level of 175
mg/dL or more has a 2.5 X 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.
There is no evidence to support bicarbonate therapy in acidemia of septic shock.
Hypocalcemia 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.
g. Inotropes

52. 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 phenylethanolamine 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

53. Epinephrine and norepinephrine raise mean arterial pressure.
Epinephrine is a potent inotrope and chronotrope, and a systemic (SAP) and pulmonary vasodilator.
Thus epinephrine preserves the SAP/PAP ratio.
Epinephrine causes adverse hyperglycemia 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,

54. 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.2 In the vasculature 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 cathecholamine.

55. 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.

56. Goal oriented Rx
of SHOCK
Septic shock PPHN Critical CHD’s
Hypo-volumia
Or
Metabolic
Respiratory support
antibiotics
Pulmonary
vasodilator
PGE1
Specific therapy
Fluid / Blood
specific therapy
ABC of resuscitation as per NLS/APLS guideline, intubate/ventilate
Rule out and Dx Pneumothorax, Cardiac tamponade, hsPDA
Normal MAP-CVP, SccO2>70%, CI 3.3-6l/sqM/min or SVC flow>40 ml/kg/min
Institue specific therapy as soon as possible AND early functional ECHO