Approach to Neonatal Shock a ppt on shock

Neonatal shock is a life-threatening condition in newborns characterized by inadequate tissue and organ perfusion due to impaired circulation. It can result from various causes such as infection (septic shock), blood loss (hypovolemic shock), heart dysfunction (cardiogenic shock), or obstruction of blood flow (obstructive shock). Early signs include poor feeding, lethargy, pale or mottled skin, weak pulses, prolonged capillary refill time, and low urine output. If left untreated, it can rapidly progress to multi-organ failure. Prompt recognition and management, including fluid resuscitation, inotropic support, and treatment of the underlying cause, are crucial to improve outcomes in affected neonates.

1. Approach to neonatal shock
Dr Aparna C, MD (PGI), DM (neo) AIIMS
Clinical director, neonatology,
KIMS Cuddles, Kondapur

2. Objectives
•Case scenarios -neonatal shock
•Shock -definition
•Hemodynamic determinants
•Vasoactive agents and their action
•Hydrocortisone

3. Case scenario 1
•Baby of A
•39 weeks/ 2900 g
•Born by prolonged NVD
•Didn’t cry immediately after birth;
•Resuscitated –12 min, PPV + intubation
•APGAR: 3/5/7
•CBG: pH-6.84; BE: -19; lactate 5 mM/L
•Intubated –SIMV 18/5, 40%

4. At 1 hour of life..
•HR:185/min
•RR:65/min
•BP:48/30 mmHg
•Peripheral pulses feeble
•CRT: 4 sec
•No seizures
•Diagnosis: Shock????
Asphyxia
Echo:
EF –25%
Poor LV function
Severe PAH
RA/ RV dilatation

5. Causes of shock in neonates -Cardiogenic
Type Of Shock Cause Clinical Clues/ Underlying conditions
HypovolemicBlood loss (placental bleed, IVH,
pulmonary hemorrhage, DIC)
Antepartum hemorrhage, h/o asphyxia,
Pallor, evidence of blood loss
Plasma loss (low oncotic pressure,
capillary leak)
Hydrops, Necrotisingenterocolitis, Sepsis
ECF loss (insensible water loss,
polyuria)
Extreme prematurity, excessive weight loss
CardiogenicMyocardial dysfunction (asphyxia,
SIRS, myocarditis, Cardiomyopathy)
Asphyxia, Infant of diabetic mother, Sepsis,
postnatal hypoxia
Decreased systolic BP, e/o cardiac failure
Arrhythmia HR> 220/mt, ECG rhythm disturbance

6. Case scenario 2
•Baby of P
•27
+2
weeks/ 840 grams
•Antenatal History
•Did not receive ANS
•Spontaneous preterm labor
•APGAR: 7/8/8
•Early CPAP started 5 cms, 30%

7. At 1 hour of life..
•HR: 135/ min
•BP 30/10 mm Hg
•CRT: 4 sec
•Cool peripheries
•SAS –3/8 on CPAP
Is the baby in shock????
Prematurity
Failure of transitional circulation
Early onset
Biventricular dysfunction
PPHNSecondary to RDS
PDA
Pathophysiology
Bad lungs –PPHN
Increased systemic after load due to loss of
placental circulation, LV dysfunction
Low SVC flow also suggesting high systemic
vascular resistance

8. Causes of shock in neonates…
Type Of Shock Cause Clinical Clues/ Underlying conditions
Distributive Peripheral vasodilatation (sepsis,
drugs, neurogenic)
Other features in sepsis –sclerema,
bleeding, lethargy
Wide pulse pressure
Vasoconstriction 1
st
24hours of life in ELBW neonates
ObstructiveObstruction of vessels (Aortic
stenosis, coarctationof aorta)
Poor lower limb pulses > upper limb pulses,
murmur
Tension pneumothorax, Cardiac
tamponade
Hyper expanded chest, decreased air entry
, carbon dioxide retention

9. Case scenario 3
•Baby of S
•37
+4
weeks/ 2900 grams/ NVD outside
•No significant antenatal risk factors
•Cried immediately after birth
•Massive lower GI bleed, pallor on day 3

10. On examination
•HR 180/mt
•Feeble pulses
•BP64/45mmHg
•CRT –could not be assessed due to severe pallor
•RR 60/mt, acidotic breathing
•pH 6.9/ HCO3 5.0/ BE -20
•USG –SMA SMV axis normal, Abd-soft Hypovolemic -
VKDB
Hb4 g%
TLC 13,000
Platelets
3,40,000
PT 30 s
PTT 69 s
Managed with one fluid bolus , repeated after 1 hour
2 units of 15 ml/kg each PRBC transfusion
Vitamin K
PIVKA –inconclusive
Hbimproved to 13.4 g% in 48 hours, bleeding stopped after 36 hours

11. Cause?...Hypovolemic shock
Type Of Shock Cause Clinical Clues/ Underlying conditions
HypovolemicBlood loss (placental bleed, IVH,
pulmonary hemorrhage, DIC)
Antepartum hemorrhage, h/o asphyxia,
Pallor, evidence of blood loss
Plasma loss (low oncotic pressure,
capillary leak)
Hydrops, Necrotisingenterocolitis, Sepsis
ECF loss (insensible water loss,
polyuria)
Extreme prematurity, excessive weight loss
CardiogenicMyocardial dysfunction (asphyxia,
SIRS, myocarditis, Cardiomyopathy)
Asphyxia, Infant of diabetic mother, Sepsis,
postnatal hypoxia
Decreased systolic BP, e/o cardiac failure
Arrhythmia HR> 220/mt, ECG rhythm disturbance
Pure hypovolemic shock is
extremely rare in neonates!!

12. Case scenario 4
•Baby of N
•38 weeks/ 3500 grams, LSCS
•Apgars-8/9, no resuscitation required
•Breast fed in ward , at 28 hours noted to have off-colour look
and cold peripheries
•Shifted to NICU

13. On examination
•RR 65/mt, retractions, SAS 2/10
•HR 175/mt
•Pulses poorly felt in LL, UL well felt
•BP (lower limb) 46/30 mm Hg
•Upper limb 86/48 mm Hg
•CVS: short systolic murmur
•Hepatomegaly
Duct dependent CHD-
coarctation
One fluid bolus
UVC established
Dobutamine10 mcg/kg/min
PE1 infusion started
Shifted for coarctation
repair

14. Case scenario 5
•Preterm, 31 w, 1.2 kg
•On GIR (UVC line) 12mg/kg/min
•In room air
•D4 -develops sudden pallor & poor CRT
•Central and peripheral pulses not felt
•BP –not recordable
•Progressive hypoxia/bradycardia
•Intubated with CPR
•Fluid bolus, epi, PG
drip started
Bedside test?
Pericardial
effusion
Cardiac
Tamponade

15. Causes of shock in neonates…
Type Of Shock Cause Clinical Clues/ Underlying conditions
Distributive Peripheral vasodilatation (sepsis,
drugs, neurogenic)
Other features–sclerema, bleeding,
lethargy
Wide pulse pressure
Vasoconstriction 1
st
24hours of life in ELBW neonates
ObstructiveObstruction of vessels (Aortic
stenosis, coarctationof aorta)
Poor lower limb pulses > upper limb pulses,
murmur
Tension pneumothorax, Cardiac
tamponade
Hyper expanded chest, decreased air entry
, carbon dioxide retention

16. Case scenario 6
•D7, Term, 2.9 kg, F
•Poor feeding: 8 h
•Drowsy, cold
•CRT 5 sec, HR 190/mt
•Mean BP 30 (<5
th
centile)
•No murmur
•No organomegaly
•No f/s/o CHD
•Hb13 gm%, TLC 10,000/, P40
L60, Plat: 1.6 l, BSL: 55 mg %
•Na 115, K 6.7
•S Creat0.5Postnatal collapse –think of duct dependent CHD, IEM, CAH
Fluids
Dopamine @ 20
mcg/kg/min
Epinephrine @ 0.5
mcg/kg/min

17. Case 6 …contd
•Started on
hydrocortisone@ 20
mg/m
2
/day in 3 divided
doses
•Flurocortisone–0.05-
0.2mg/m2/day
•Infants with crisis-
rehydration with NS
•Inotropes tapered
•Sodium supplements –
10 mEq/kg/d
•K chelators

18. Shock
Acute, complex state of circulatory dysfunctionresulting in
insufficient oxygen and nutrient delivery to meet tissue
requirements

19. Blood pressure = Cardiac output x Systemic vascular resistance
Heart rate and stroke volume Neuroendocrine and paracrine
Regulatory mechanisms
Arrhythmias Preload ContractilityAfterload
High afterload
Low afterload
Poor contractility
Hyperdynamic
precordium
Hypovolemia
Diastolic dysfunction
Volume overload
Vasoconstriction
Vasodilatation
Determinants of hemodynamic status

20. Normal hemodynamics
Preload
Contractility
Afterload
Heart rate
Cardiac
output
Hemoglobin
Blood
pressure
SVR
O
2 Saturation
O
2
content
O
2Delivery

21. Abnormal hemodynamics
Low vascular
resistance
Vasodilation
Sepsis
SIRS (NEC)
Enlarged vascular bed
HSPDA
AV Malformation
Bronchopulmonary
sequestration

22. Abnormal hemodynamics
Myocardial
contractility
Myocardial injury
Asphyxia
ALCAPA
Cardiomyopathy
(viral / metabolic/ drug)
Myocardial dysfunction
Septic shock
Post PDA ligation
HLHS
Prolonged
tachyarrhythmia

23. Abnormal hemodynamics
Reduced
preload
Impaired filling
Hypovolemia
HOCM
Cardiac tamponade
Tension pneumothorax
Low PBF
High MAP
Obstructed PV
PPHN
RV dysfunction
Decreased
contractility

24. Abnormal hemodynamics
Increased
afterload
Failed adaptation
Removal of placenta
Post PDA ligation
Vasoconstriction
Exogenous
vasopressors
Cold septic shock
Decreased
contractility

25. Abnormal hemodynamics
Heart rate
Persistent bradycardia
Congenital heart
blocks
Persistent tachycardia
SVT
Atrial flutter

26. Detection of Shock
•Central–peripheral temperature
difference
•Central venous pressure
•In specific scenarios
–Hepatomegaly
–New onset crepitation
•Sensorium
•Lab
–pH/BE/Lactate/SVCO
2
BP
HR
UO
Lactate
CRT

27. Detection of shock
NoParameter Comments
1Colour Subjective, influenced by light,Hb, race
2CRT Normal < 3 sec; Maybe delayed in hypothermia, base of sternum
preferred
3Core-
peripheral∆
temp
Normal < 2 degC;
Influenced by temperature, vasoactivedrugs
4HR Increasedin fever, anemia, pain, agitation, drugs, arrhythmia
Influences CO and myocardial perfusion
5BP Late sign –decompensated shock; Determinedby CO& SVR
6UrineoutputLate marker –indicatesrenal perfusion
No one reliable sign!!
Combination of signs is more informative

28. Bedside monitoring
Clinical
parameters
1.Heart rate
2.Capillary refill time
3.Blood pressure
4.Urine output
5.Sensorium
6.Core peripheral TD
7.Blood lactate & gas
Gadgets
Pulse oximetry –HR, SpO2, PI, PVI
Echocardiography
•Preload –IVC collapsibility, LV volume
•Contractility –eye ball, FS, EF
•Systemic perfusion –LVO, RVO, SVC flow
Electrical velocimetry, NIRS

29. Volume status -IVC collapsibility

30. Contractility -M mode -FS

31. Clinical and physiological variables

32. Detection of Shock
Data based on preterm VLBW infants with low perfusion as assessed by ECHO
BP and CRT are imperfect bedside tests for detecting low blood flow on day 1
Osborn 2004

33. Management of shock
1.Correct hemoglobin
2.Reduce work of breathing –mechanical ventilation
3.Correct hypoglycemia
4.Correct hypocalcemia
5.Correct acidosis
Fluids, vaso active drugs, hydrocortisone, PGE1

34. Fluid resuscitation
•Mainstay in the resuscitation of patients with septic shock
•Marked hypovolemiamay result from vasodilatation and increased
capillary leak
•Maintenance of preload and tissue perfusion
Caution !!!!
Preterm –PDA, IVH
◦Remember !!!!
◦Hypovolemia not a common cause of hypotension in NB

35. Fluid resuscitation –crystalloid vscolloid
•No benefit of 5% human
albumin solution over
0.9% NaClin hypotensive
preterm infants
•Cochrane –Crystalloids
are the answer!
So KW, Dis Child Fetal Neonatal Ed 1997;76:F43-6
Correction
Acidosis, hypoglycemia,
hypocalcemia

36. Vasoactive drugs
AGENT α1 α 2 β1 β2 Dopa
Increase
contractility
Peripheral
vasoconstriction
Incrate
Incconduction
Inccontractility
Peripheral
vasodilatation
Renal,mesenteric
and coronary
vasodilatation
Dobutamine + ++++ ++ 0
Dopamine ++/+++ ? ++++ ++ ++++
Epinephrine++++ ++++ ++++ +++ 0
Norepi.rine+++ +++ +/++ 0 0
Caution: adrenergic receptor ontogeny in preterm neonates
Lower GA: αadrenergic receptors –denervation hypersensitivity α2 >>α1
Later GA: βactivation –β2 >>β1
Watch for increase in SVR (BP) in preterm neonates!!

37. Dopamine
•Vasodilatation in kidneys,
Intestine, coronary arteries
•Increase in GFR
•Direct renal tubular effects
Alpha receptors
α1 >α2
Beta receptors
β1 only
Dopamine
receptors
Renal ,mesentery,
coronary
•Positive inotropy
•Positive chronotropy
•Peripheral vasodilatation
•Vasoconstriction
•Positive inotropy
Medium doses 2-
6µg/kg/min
High doses 6-10
µg/kg/min
Naturally occurring catecholamine, precursor of epinephrine and norepinephrine
Dopamine

38. Dobutamine
•Has an asymmetric carbon atom with two enantiomers
•Positive Isomer has effects on β1 and β2 effects
•Main metabolite of dobutamine, (1)-3-O-methyl-dobutamine, exerts α 1-
receptor inhibitory effects
•Net effects
•Increases in myocardial contractility and, to a lesser extent, heart rate,
and either no effect or a decrease in SVR

39. Epinephrine
•Very useful as ionotropiceffect
•Increased vascular resistance at higher doses
•Dosage 0.1 to 0.3 µg/kg/min
•Caution in premature infants

40. Nor epinephrine
1.Acts on vascular & myocardial α-1 receptors [α-1 (> β-1 > β-2)]
2.Alpha receptor activity –vasoconstriction (predominant)
3.Beta receptor activity –inotropic, chronotropic (minimal)
4.Dose range –0.1 to 0.5 mcg/kg/min
•Net effects
•Increases in SVR (BP)and myocardial contractility

41. Milrinone
•PDE 3inhibitor
•Exerts its cardiovascular effects through the inhibition of cAMP
degradation
•Effects
–Enhances myocardial contractility
–Promotes myocardial relaxation
–Decreases vascular tone in the systemic and pulmonary vascular beds
–Causeshypotension
•Dose: 0.25–1.0μg/kg/min
Cardiogenic shock with
PPHN component

42. Vasopressin
1.Endogenous neuropeptide –posterior pituitary
2.Regulation of plasma osmolarity, circulating blood volume and vascular
tone
3.V1a (>V2) receptors agonism—vasoconstriction
4.Fluid retention & hyponatremia
5.Dose range –0.0002–0.005 U/kg/min

43. Inotropes in neonates

44. Inotropes in neonates

45. Inotropes

46. Role of hydrocortisone
Genomic effects :
•Increase in the rate of a-and b-
adrenoreceptorand adenylatecyclase
gene transcription
•Increased density of a-and b-
adrenoreceptorsand enhanced expression
of adenylatecyclase
•Inhibition of iNOSgene activation and
cytokine/chemokine production
Non-Genomic effects :
▪Inhibition of catechol-0-methyltransferase
(COMT) and nor epinephrine reuptake
▪Increase in intracellular calcium availability
▪Improved capillary integrity due to
decreased cytokine/ chemokine
production
Shock dose is 25 times higher than stress dose.
(Hydrocortisone dose =1-2 mg/kg/dose 8 hourly)

47. Dosing guide
Medication Syringe Dose in mg/kg
in 24 ml
Rate of infusionDelivered dose
at mcg/kg/min
Dopamine
(1ml=40 mg)
50 ml 14.4 1ml/hr 10
Dobutamine
(1ml=50 mg)
50 ml 14.4 1 ml/hr 10
Adrenaline
(1ml=1mg)
20 ml 1.44 1 ml/hr 1
Milrinone 50 ml 1.5 mg/kg to 50
ml
1 ml/hr 0.5
PGE1
(1ml=500 mcg)
1 ml added to
50 ml
-- 0.6 ml/kg/hr 0.1

48. Algorithm
End points
1) Normal heart rate, CFT≤ 2 s,
and BP within norms (first hour)
2) Restore normal perfusion
pressure (mean arterial pressure –
central venous pressure)
3) Preductal and postductal
oxygen saturation difference < 5%
4) either Scvo2 > 70% (* except
congenital heart disease with
mixing), SVC flow > 40 mL/kg/min
Hydrocortisone 25 mg/m2/day in
catecholamine resistant shock

49. Case 1 -Hypoxic ischemic injury
Pathophysiology
1.LV dysfunction
2.RV dysfunction
3.PPHN
Management
1.Positive inotropic agent –
Dobutamine / Milrinone
1.Positive inotropic agent –Epinephrine
2.Prostaglandin (if restrictive or no DA)
3.Hydrocortisone if refractory
4.Selective pulmonary vasodilator

50. Case 2 -ELBW transitional circulation
Pathophysiology
1.Large PDA
2.LV Systolic dysfunction
3.Diastolic dysfunction
Management
1.Positive inotropic agent –
Dobutamine / Milrinone
1.Positive inotropic agent –Epinephrine
2.COX inhibitors(if hs-PDA)
3.Hydrocortisone if refractory

51. PPHN
Pathophysiology
1.Low LV preload
2.Right to Left shunt
3.LV systolic
dysfunction
4.RV systolic
dysfunction
Management
1.Lung recruitment
2.Correct all reversible causes
3.Pulmonary vasodilators
4.Inodilators –Dobutamine, Milrinone
1.Vasopressin/ noradrenaline if low MAP
2.Prostaglandin (if restrictive or no DA)

52. Case 3: Congenital CHD
Pathophysiology
1.LV dysfunction
2.Syst. Hypertension
3.PPHN
Management
1.Correct acidosis
2.Inodilators –Dobutamine, Milrinone
3.Prostaglandin (if restrictive or no DA)
4.Lasix if CCF/ hepatomegaly
1.Adrenalineif low MAP

53. Case 4: Post PDA ligation
Pathophysiology
1.SVR
2.Syst. Hypertension
3.LV dysfunction
4.BPD
Management
1.Optimise ventilation
2.Inodilators –Dobutamine, Milrinone
3.Lasix if CCF/ hepatomegaly
1.Hydrocortortisone for adrenal
insufficiency

54. Take home messages
•Shock –failure to meet the tissue oxygen demand
•Understanding normal & abnormal hemodynamics –key to treatment
•Clinical indicators –unreliable
•Echo –useful in optimizing the treatment
•Supportive care –mandatory for all shock cases
•Cardiac medication –titrate as per underlying hemodynamics

55. Thank You!