This document summarizes shock in newborns. It discusses definition, pathophysiology, types including hypovolemic, cardiogenic, septic, and distributive shock. Signs and symptoms are tachycardia, decreased blood pressure, prolonged capillary refill time, and decreased urine output. Management involves supportive care, fluid resuscitation, and inotropic drugs like dopamine, dobutamine, and epinephrine to increase cardiac output depending on the cause of shock. Close monitoring is needed to guide therapy and prevent complications.

1. Welcome to Seminar
Dr.Olivia Akther(Year 2)
Paediatric Hematology & Oncology
Dr.Md. Sazzadul Alam (year 3)
Resident
Department of Neonatology
BSMMU

2. Case summary
• S/O Srabony Term(38 weeks) LBW(2090 gm)
SGA with Late onset of neonatal sepsis, at D5
baby developed less activity
O/E- Reflex activity poor,CRT-4 sec, Low pulse
volume, BP 70/42(51), HR-178/min,RR-70/min,
Temp 36.7 C, CBG -4.4 mmol/L, Urine output
decreased, other findings normal

3. Assessment
Septic Shock

4. Case summary
• S/O Yasmin, Term(37 weeks) LBW(2170 gm)
AGA with PNA with IDM, at D7 baby
developed Tachycardia & tachypnoea
O/E- Reflex activity good,CRT-4 sec, Low pulse
volume, BP 66/48(54), HR-186/min,RR-69/min,
Temp 37.2 C, CBG -5.1 mmol/L, CVS-Systolic
murmer in left upper sternal border,
Hepatomegaly 3 cm RCM,Urine output
decreased, other findings normal

5. Assessment
Cardiogenic Shock

6. Shock in Newborn

7. Contents
• Definition
• Consequence of Shock
• Pathophysiology
• Stages of Shock
• Types of Shock
• Etiology
• Sign and Symptoms of Shock
• Laboratory tests
• Management
• Key Points

8. Definition
• Shock is defined as acute circulatory
dysfunction result in insufficient oxygen &
nutrient delivery to the tissues relative to their
metabolic demand, leading to celluler
dysfunction that may lead to lactic acidosis &
if left to untreated causes cell death.
Cloherty & stark’s manual of neonatal care-8th edition

9. Consequence of Shock
Inadequate oxygen and nutrient substrate
delivery
Compromised metabolic waste removal
Cellular dysfunction and death
May involve isolated organs or entire organism

10. Pathophysiology

11. Inadequate tissue perfusion may result from:
1. Defects of the pump = (cardiogenic)
2. Inadequate blood volume = (hypovolemic)
3. Abnormalities within the vascular beds =
(distributive)
4. Flow restriction = (obstructive)
5. Inadequate oxygen-releasing capacity = (dissociative).

12. Hemodynamics
Myocardial
Contractility
StrokeVolume Preload
CardiacOutput Afterload
Blood
Pressure HeartRate
SystemicVascular
Resistance

16. Stages of Shock
Clinical parameter Stagel Stage ll Stage lll
Heart Rate Tachycardia Marked Tachycardia Severe Tachycardia,
Bradycardia
Respiratory rate Normal Tachypnea Tachypnea/Apnea
BP Normal Hypotension Severe Hypotension
Pulse pressure Normal Low Markedly Low
Skin Cool Mottled Cold & cyanotic
Mental status Anxious Obtunded Coma
Urine Normal Oliguria Anuria

17. Types of Shock
Hypovolemic
Cardiogenic
Distributive
Septic
Neurogenic
Anaphylactic
Obstructive
Dissociative

18. Hypovolemic shock
Intrapartum Hemorrhage
Placenta previa/abruption
Umbilical cord injury
Twin-twin transfusion
Maternal-fetal hemorrhage
Fetal hemorrhage

19. Hypovolemic shock
• Postpartum Hemorrhage
Coagulation disorders
Vit K deficiency
Brain hemorrhage
Lungs
Adrenal glands
Scalp

21. Cardiogenic Shock
• Congenital heart disease
• Arrhythmia
• Severe hypoglycemia
• Asphyxia
• Bacterial or viral infection
• Severe metabolic/electrolyte abnormalities
• Hypoxemia and metabolic acidosis

22. Endotoxemia
Release of vasodilator substance
Hypotension
Septic shock

23. Pathophysiology of septic shock

24. Neurogenic shock
Secondary to decreased
sympathetic activity.
Decreased vascular tone.
Vasodilatation with decreased
tissue perfusion

25. Anaphylactic shock
Hypersensitivity reaction.
↓
Vasodilation and increase capillary
permeability.
↓
Fluid shift with severe hypotension.
↓
Circulatory collapse

26. Obstructive shock
• Any obstruction to venous blood return.
• e.g-Tension pneumothorax,
• Pericardial tamponade,
• Diaphramatic hernia,
• Air embolism,
• Aortic stenosis, Coarctation of aorta,
• Hypoplastic left heart syndrome.

27. Dissociative shock
• Inadequate oxygen-releasing capacity
 severe anemia,
 methemoglobinemia.

28. Sign and Symptoms of Shock
Altered level of consciousness
Tachycardia, decreased SBP and pulse pressure
Rapid shallow breathing
Cold, pale, clammy, diaphoretic, cyanotic skin,
decreased capillary refill time.
Decreased urine output

30. Sign and Symptoms of Shock
Features of cardiogenic shock are –
tachycardia,
tachypnea,
Hepatomegaly
Cardiomegaly
heart murmur
narrow pulse pressure
basal crackles
Peripheral edema and raised JVP are relatively
uncommon in the neonate

31. Signs of shock
• Perfusion
– Prolonged capillary refill > 3 seconds
– Cool
– Mottling

32. Capillary Refill

33. Mottled skin in Neonate

34. Laboratory tests
• Complete blood count
o Hct, WBC, PLT
• Coagulation tests PT, APTT
• Arterial blood gases
• Chest x-ray,ECG
• Echocardiogram
• CVP
• Serum lactate,Histamine

35. Laboratory tests
• Electrolytes
• BUN/creatinine and urinalysis
• hepatic function tests
• Newer non- invasive tools-
– functional echocardiography (FE)
– near infrared spectroscopy (NIRS)

36. Management

37. Goals of therapy
Normal mentation
Normal heart rate for age
Normal pulse and blood pressure
Capillary refill of less than 2 s
A urine output of more than 1 ml/kg/h

38. Management
1. Supportive:
Correction of -
Hypoxia
Acidosis
Hypoglycemia
Hypocalcemia
 Provide respiratory support
High flow O2
CPAP
Mechanical ventilation

39. Management
2. Rule out causes that require immediate
treatment
Pneumothorax- Chest tube
Cardiac tamponade-pericardiocentasis
Duct dependent lesion- prostaglandin
3. Determine the cause of shock –
volume replacement or inotropic agents

40. Management
a. History-
 Birth asphyxia
 Blood loss- antepartum or postpartum
 Drug infusion
 Birth trauma-liver injury

41. Management
b. Physical examination-
Features of cardiogenic shock are –
tachycardia,
tachypnea,
Hepatomegaly
Cardiomegaly
heart murmur
narrow pulse pressure
basal crackles
Peripheral edema and raised JVP are relatively
uncommon in the neonate

42. Management
c. Chest x-ray-
 Small heart- volume depletion
 Large heart-cardiac disease
d. Central venous pressure
 Volume depletion
 Preterm - < 4mm of Hg
 Term- < 5mm of Hg
 Cardiogenic shock.
 Preterm - > 6mm of Hg
 Term- >8mm of Hg

43. Management
e. Echocardiogram-
LVO- Normal or high- Vasopressor ( Dopamine)
LVO- Low and left ventricle show under filling-
Volume expansion
LVO- Normal and left ventricle show impaired
contraclity- Dobutamine

44. If still the cause is uncertain-
Management
N/S -10 mL/kg over 30 min
no responseresponse
inotropic agentcontinue volume
expansion

45. Management
The first step - volume expander
The second step - Inotrops and vasopressor
The third step - steroids

46. Fluid therapy
 Single most important intervention in patients presenting
with hypovolemic shock
 Crystalloids (Normal saline) are preferred over
colloids(Albumin)-
 they are more readily available
 have lower cost
 lesser risk of infectious complications

47. Fluid therapy
In previous years, clinicians have administered colloids,
such as albumin, in order to replace the intravascular
loss.
However, studies have proven that:
 When albumin and crystalloids (normal saline)
are compared in terms of cost, availability,
safety, and effective therapeutic outcome,
normal saline becomes the agent of choice for
volume expansion.
• Oca MJ, Nelson M and Donn SM (2003): Randomized trial of normal saline versus 5% albumin for
thetreatment of neonatal hypotension. J Perinatol;23(6):473-476

48. Term infants- 10 mL/kg over 5 - 10min, can be
repeated upto 40 to 60 ml/kg until perfusion
improves or hepatomegaly develops
Preterm infants- 10 mL/kg over 10 – 30 min,
can be repeated
Blood cell transfusions or fresh frozen plasma
are recommended in cases of blood loss or
DIC

49. Fluid therapy
 Infants with cardiogenic shock-
 Careful assessment of the fluid status should be done
Volume loading the failing heart may exacerbate
pump failure and contribute to pulmonary congestion
Ideally, a central venous line should be placed to
monitor CVP and to assist in adjusting therapy

50. Commonly used inotropes and vasopressor
1. Adrenergic receptor agonist
 Adrenaline
 Noradrenaline
 Dopamine
 Dobutamine
2. Phosphodiesterase Inhibitor
 Milrinone
 Amrinone
3. Vasopressin

51. Adrenergic receptors
Receptor Site Action
α1 Smooth muscles in BVs Vasoconstriction of coronary arteries
Vasoconstriction of peripheral veins
α2 Pre and postsynaptic nerve
terminals
Vasoconstriction of coronary arteries
Vasoconstriction of peripheral veins
Increased myocardial conduction velocity
β1 Cardiac muscles Increase in heart rate
Increase in contractility
β2 Blood vessels
Bronchi
Dilates smaller BVs
Dilates the arteries of skeletal muscles
bronchodilatation
Dopaminergic 1 Splanchnic circulation ,
Kidney
Renal and mesenteric vasodilatation
Dopaminergic 2 splanchnic circulation,
Kidney
Renal and mesenteric vasodilatation

52. CVS effect of vasopressor & ionotrops(Physiological goal)
Dose
μg/kg/min
Receptor
stimulated
Primary
indication
Potential CVS
adverse effect
Increase cardiac output
Dobutamine 5-20 Β1,β2α1 Cardiac
dysfunction
Tachycardia
Sys. VD
Increase cardiac output & decrease pulmonary vascular resistance
Milrinone 0.33-1 PDE3 inhibitor Cardiac
dysfunction &
PPHN
Systemic
Hypotension
Increase cardiac output & systemic vascular resistance
Dopamine 0.5-2 Dopaminergic Poor urine out Tachycardia,
Pulmonary
vasoconstrictio
n
2-6 Β1,dopa Cardiac
dysfunction
>6 Α1, Β1,dopa Hypotension

53. CVS effect of vasopressor & ionotrops(Physiological goal)
Dose
μg/kg/min
Receptor
stimulated
Primary
indication
Potential CVS
adverse effect
Epinephrine 0.05-0.1 Β1,β2 Cardiac
dysfunction
Tachycardia,
Lactic acidosis
Hyperglycaemi
a
0.1-0.5 α1, α2Β1,β2 Hypotension
refractory to
dopamine
Increase systemic vascular resistance
Vasopressor 0.1-1.2
mU/kg/min
V1,V2 Hypotension Hyponatraemia

54. Dopamine
 Dopamine activates receptors in a dose-dependent
manner:
Low dopamine dosages- (1-5 μg/kg/min)
stimulates peripheral dopamine receptors and increased
renal, mesenteric, and coronary blood flow
little effect on CO
Medium dosages (5-15 μg/kg/min)- has positive
inotropic and chronotropic effects (β1 and β2)
High dosages (≥15 μg/kg/min)- stimulates α1 and α2
adrenergic receptors, resulting in VC and increased PVR
• Gomella TL, Cunningham MD, Eyal FG and Zenk KE (2004): Neonatology:Management,
Procedures, On-Call Problems, Diseases, and Drugs. 5th ed. Stanford, CT: McGraw-Hill

55. Dopamine
The established dose ranges of 2-20
μg/kg/min
For the initial management a 5-10
mcg/kg/min dose is recommended
The dose is generally incremented by 2.5
mcg/kg/min every 10-15 minutes
Roze JC, Tohier C, Maingueneau C, Lefevre M and Mouzard A (1993): Response to dobutamine and dopamine in
the hypotensive very preterm infant. Arch Dis Child;69:59-63

56. Dopamine
 Dilute full-strength injection before administering.
 Compatible solutions: normal saline solution, D5W, 5%
dextrose and half-normal saline solution, 5% dextrose and
normal saline solution, , lactated Ringer’s solution
 Do not add to sodium bicarbonate solution or other
alkaline solutions, because this inactivates drug.
 Infuse into large (preferably central) vein
 Never stop infusion abruptly, as this may cause severe
hypotension. Taper gradually

57. Dopamine
Side effects of dopamine:
1. Extravasation causes tissue necrosis (infusion
site should be monitored).
2. Ventricular arrhythmia,
3. Ectopic heartbeats
4. Tachycardia
5. Hypertension.

58. Dobutamine
 It has a greater affinity for the β receptors on the
myocardium producing a stronger left ventricular
contraction.
 Dose- 2 to 20 mcg/kg/min
 Adverse effects of dobutamine include-
 Arrhythmias,
 Hypotention if hypovolemic
 Elevated BP
 Ectopic beat

59. Epinephrine
Epinephrine as a pharmacological agent
increased both BP and CO by stimulating the α
and β receptors.
 Low dose (0.05 to 0.3mcg/kg/min)-epinephrine
stimulates the β receptors causing a positive
inotropic and chronotropic effect.
Higher doses - which stimulate the α receptors in
the peripheral vasculature causing increased BP

60. Epinephrine
 Dose- 0.1 to 1 mcg/kg/min
 Adverse effects-
Hypertention
Tachycardia
Pallor
Increased myocardial O2 consumption
Decrease renal blood flow

61. Norepinephrine
Norepinephrine use is limited because of its
prominent VC activity, which raises concerns
about:
1. Possible ischemia
2. Afterload
3. Myocardial oxygen demand
4. RBF and UO

62. Hypovolemic Shock
Can be repeated upto 40 – 60 ml/kg untill perfusion
improved or hepatomegaly develope
Term- 10ml/kg over 5-10 minutes
Volume expansion with normal saline

63. Hypovolemic Shock
Then reassess and Dopamine can
be given if needed
Pre-term- 10ml/kg over 10 – 30
minutes
Blood replacement if Hct < 30 – 35%( PRBC- 5 to 10 ml/kg)

64. Cardiogenic Shock
 First, treat any obvious cause.
 Arrhythmia
 Metabolic cause.
 Asphyxia.
 The goal is to improve cardiac output. Inotropic
agents should be used intravenously
 Volume expansion is not needed and may be harmful
 Dopamine- Drug of choice and superior to
dobutamine

65. Cardiogenic Shock
 Dobutamine-
If dopamine fails to improve BP, dobutamine is
recommended as a secondline drug.
In neonates, it is usually given together with
dopamine infusion
 Other agents-
Epinephrine
 Milrinone

66. Septic Shock
1. Initiate empiric antibiotic therapy – after culture
specimens have been obtained.
2. Volume replacement-
In term infants or older preterm infants,
aggressive volume expansion (push boluses of
10–40 mL/kg up to 60mL/kg over 20 to 30
minutes should be considered (Carcillo et al 2002).

67. Septic Shock
Cardiovascular agents-
 A delay in administration of inotropes was associated with
a 20-fold increased mortality risk (Kisson et al 2010)
 Dopamine- remains the first-line agent in neonates, and
epinephrine may be used in dopamine-resistant septic shock
(Carcillo et al 2002).
 The initial dose of 5-10 mcg/kg/min is recommended and
incremented by 2.5 mcg/kg/min steps every 10-15 minutes
(Pellicer et al 2009).

68. Septic Shock
 If no improvement-
 Dobutamine- 2.5-10 mcg/kg/min,
 Epinephrine- 0.05– 0.3 μg/kg/min)
 Norepinephrine- Use is limited in neonatal shock. It
is indicated for “warm” shock, an uncommon
condition in the newborn.

69. Septic Shock
. Corticosteroids
 Corticosteroids are often used to treat shock when
volume expansion and inotropes are ineffective to
raise blood pressure.
 They may act by-
 improving the vessel wall sensitivity to circulating
cathecolamines or to exogenous vasoactive drugs,
inhibiting the nitric oxide synthase enzyme expression, or
suppressing immune responses.
Additionally, septic newborns may develop relative adrenal
insufficiency

70. Term(ACCCM)
Shock(Airway
, establish
access
accordingly)
• Fluid resuscitation 10ml/kg upto 60 ml/kg
• Correct hypoglycemia,Hypocalcemia,beg. Antibiotic,PG
Fluid
refractory
Shock
• Dopamine 5-9 μg/kg/min
• Add Dobutamine 10 μg/kg/min
Fluid
refractory
dopamine
resistant shock
• Epinephrine 0.05-0.3 μg/kg/min
Catecholamin
e resistant
shock
• CVP, ScvO2, SVC, CI
Cold shock, normal
BP, poor LV
function- Volume
loading, vasodilator,
(milrinone)
Cold shock, Low BP,
poor RV dysfunction-
PPHN Inhaled NO,
milrinone, inhaled
iloprost, I/V adenosine
Warm shock with Low BP- Add
volume, norepinephrine,
vasopressine, terlipressine,use
ionotropes
Ref. shock ECMO

71. Preterm(ACCCM)
Shock(Airway
, establish
access
accordingly)
• Fluid resuscitation 10ml/kg upto higher amount needed
• Correct hypoglycemia, Hypocalcemia,beg. antibiotic, PG
Fluid
refractory
Shock
• Dopamine 5-10 μg/kg/min,Higher dose or add of epine may needed
• Add Dobutamine 10 μg/kg/min upto 20 μg/kg/min if CD dysfun.
Fluid
refractory
dopamine
resistant shock
• Epinephrine 0.05-0.3 μg/kg/min ,remain hypotensive-HC(1mg/kg)
Catecholamin
e resistant
shock
• MAP,Perfusion,U/O
Cold shock, normal
BP, poor LV
function-
(milrinone) If
normal Renal funct.
Cold shock, Low BP,
poor RV dysfunction-
PPHN Inhaled NO,
milrinone,
Warm shock with Low BP-
vasopressine, terlipressine with
ionotrps
Ref. shock ECMO

72. Therapeutic end points
 Capillary refill of less than 2 s
 Normal pulses with no differential between peripheral
and central pulses,
 Normal heart rate
 Warm limbs
 Urine output of more than 1 ml/kg/h
 Normal mental status
 Improved base deficit
 Decreased lactate

73. Future perspective
 Endotoxin-neutralizing therapies- Recent studies in
children with septic shock with endotoxin-neutralizing
therapies reported reduction in mortality with recombinant
human bactericidal proteolytic increasing factor and HA-1A
antibody.
 Terlipressin- a long acting vasopressin analog, stimulates
vascular V1a receptors, resulting in vasoconstriction. A recent
study reported improved hemodynamic indices and renal
function in critically ill children

74. Remember
Recognize compensated shock quickly- high index
of suspicion
 Tachycardia is an early sign
Hypotension is late and ominous
Administer adequate amounts of fluid rapidly
Correct electrolytes and glucose problems
quickly.
If patient is not responding the way you think
broaden your differential, think about other types
of shock.

75. Thank You