Pediatric shock & it's management

1. Presentors: Dr. ROHIT
Dr. SAGAR
Moderator Dr. JEETENDRA

2. DEFINITION
 Shock is a clinical state characterised by inadequate
tissue perfusion resulting in imbalance between
oxygen delivery(DO2) and oxygen consumption(VO2)

3. Types of shock
 Hypovolemic
 Cardiogenic
 Obstructive
 Distributive

4. Pathogenesis
Hypovolemic Septic Cardiogenic
Third spacing Myocardial depression
Preload Vasodilation Contractility Lusitrophy
Cardiac Output

5. HYPOVOLEMIC SHOCK
MAP = CO(HR x Stroke Volume) x SVR
Decreased Intravascular volume (Preload) leads to
decreased Stroke volume
Hemorrhagic – trauma, GI bleed
Hypovolemic – Burns, GI losses, dehydration, third
spacing (e.g. pancreatitis, bowel obstruction), DKA

6. Distributive
MAP = CO (HR x SV) x SVR
Loss of vessel tone
Inflammatory cascade
1. Sepsis and TSS, Anaphylaxis
2. Post resuscitation syndrome( cardiac arrest)
Decreased sympathetic nervous system function
Neurogenic- C spine or upper thoracic cord injuries
Toxins – Due to cellular poisons – CO, MetHb, cyanide

7. Cardiogenic Shock
MAP = CO ( HR x Stroke Volume) x SVR
Decreased contractility( Myocarditis, CMP, Post
resuscitation syndrome after arrest)
Mechanical Dysfunction – ( Papillary muscle rupture
post- MI, Severe AS, rupture of ventricular aneurysms
etc)
Arrhythmia- ( Heart block, VT, SVT, AF etc)
Cardiotoxicity (B blocker and Calcium Channel
Blockers Overdose)

8. Obstructive
MAP = CO (HR x Stroke Volume) x SVR
Heart is working but there is a block to the outflow
1.Massive pulmonary embolism
2. Aortic dissection
3. Cardiac tamponade
4. Tension pneumothorax
Obstruction of venous return to heart
Vena cava syndrome- e.g. neoplasms, granulomatous
disease.

9. Physiologic profile of shock
Types of
shock
Preload Cardiac
output
Afterload
(SVR)
Tissue
perfusion
( Mixed
venous
saturation)
Hypovolemia
Distributive /
Cardiogenic
Obstructive

10. Stages of shock
Clinical
Paramter
Stage I
(Compensated)
Stage II
( Organ
Hypoperfusion/
Decompenated)
Stage III
( End organ
Failure/
Irreversible)
Mental state Clear but anxious Confused or
restless
Apathetic or
comotose
Skin Pale, cold Cold clammy Cold, cynotic and
mottled intensive
Peripheral
vasoconstriction
Mild marked marked
Blood pressure normal/ slightly
elevated
Low unrecordble
Urine output Normal/low oliguria Anuria
Heart rate increased increased increased
Respiratory rate increased Respiratory faliure Respiratory failure

11. Metabolic
change
Respiratory
alkalosis
Lactic acidosis Severe metabolic
acidosis
Basis for staging Activation of
compensatory
mechansisms
Compensatory
mechanisms
beginnings to fail
Multiple organ
failure

12. Why do we need to recognize
septic shock early??
 In septic shock time is extremely crucial!!
GOLDEN HOUR
1. 1st hr following dx of severe sepsis and shock
2. Improved survival rate and reduced organ
dysfunction if managed within this period
3. Usually this period is lost due to delayed
1.Recognition
2.Delay in transport
3.Delay in initating treatment.

13. Recognition of Shock
 Tachycardia- an important early finding in response to
low CO
 Tacypnoea
 Poor central/peripheral pulses
 Cold extremities
 Prolonged CFT
 Narrow pulse pressure
 Hypo/hyperthermia
 Hypotension-late manifestations of low CO prevented
by tacycardia and vasocontriction

14. Signs of End organ hypoperfusion
 Altered mental status- Agitation, anxiety, lethargy.
 Urine output- oliguria, Anuria.
 Skin- cool, mottled, cyanotic.
 GIT- sluggish bowel sounds, altered gastric aspirates.
Shock- primarily is a clinical diagnosis; requires a
high index of suspicion

15. Warm vs cold septic shock
Warm shock Cold Shock
Vasodilation- low SVR and high
CO
Vasoconstriction- low CO and
high SVR
Warm erythematous peripheries Cold peripheries
Flush/ instantaneous CFT Prolonged CFT
Bounding pulses Poor peripheral pulses
Wide pulse pressure Narrow pulse pressure
E.g. Distributive shock E.g. septic/ Cardiogenic

16. Blood Pressure
 Defining hypotension (SBP)
Hypotension is not synonymous with shock
Compensated shock- Normal BP with signs of poor perfusion
Hypotension is a late sign
Fall in SBP >10mmHg is worrisome even if hypotension is absent
Shock should be recognized and intervened in compensated stage
AGE FORMULA (SBP)
Term neonates < 60 mmHg
Upto 1 year < 70 mmHg
1-10 years 70 + Age in years x 2
> 10years < 90

17. Capillary Refill time
 Capillary refill time is a sensitive indicator of poor
peripheral tissue perfusion.
 Method- CRT is determined by blanching an area of
skin over the finger tips in an older child and
forehead or sternum in infants, by firm compression
with the finger-tip for 5 seconds and then noting the
time for blanching to disappear.
 CRT which takes 3 seconds or longer is an indicator of
tissue hypoperfusion.
 CRT is brisk in warm shock.

18. AVPU scale
AVPU GCS SCORE
Alert 15
Voice 13
Pain 8
Unresponsive 6

19. General management
 Hypoxemia should be prevented and corrected
 Endotracheal intubation is recommended in all cases where
shock is not readily reversible
 Vascular access should be estabilished as early as possible
 Fluid bolus remains the corner stone in conditions of overt
blood loss and hypovolemia
 Optimization and stabilization of cardiac output and SBP by
manipulating the preload, heart rate, myocardial contractility
and after load by using vasoactive and inotropic agents
 Careful monitoring.

20. Hypovolemic shock management
 Genernal management principles should be followed
first ( oxygen therapy/ rapid estabilishment of venous
access)
 In hypotensive patient Crystalloids-initial fluid of
choice in resuscitation
 20ml/kg quickly over 5-10 minutes( Target max upto
60ml/kg) and patient is reaccessed for further boluses
 If child is severely dehydrated/ compensated shock,
WHO guidelines for mangement of severe dehydration
should be initiated.

21.  If hepatomegaly or crepts develop fluid resuscitation
should be stopped.
 Colloids used in
1. Hypoproteinemic state
2. Haemorrhagic shock, coagulopathy
3. Refractory hypovolemic shock.
Types
1. 5% albumin
2. 10% dextran

22. Cardiogenic shock management
Cardiogenic shock( poor perfusion with systemic and
pulmonary congestion)
Inotropic support( Milrinone). Start diuretic consider
positive pressure ventilation( invasive/non invasive)
Is the perfusion ( CFT, pulse volume, lactate) and urine
output improved ?

23.  YES NO
Wean inotropes over 48-72hrs Add epinephrine &
& cardiology consultation titrate, optimize ventilator
for further care and PEEP
No improvement
Consider for extracorporeal life support

24. Septic shock management
 In septic shock management 1st 60minutes is called the
golden hour.
At 0 minutes
1.Recognise depressed sensorium & poor perfusion in a
febrile child.
2.Oxygen by non rebreathing mask if effortless
tachypnea and shock.
3. If airway insecure/bradypnea/apnea: Early intubation

25.  At 5min:
 Establish IV/IO access
 Withdraw emergency samples, including CBC,
electrolyte, RBS, Blood gas, Blood culture
 Only if BP< 5th centile for age: Start fluid bolus 10-
20ml/kg over 15-20ml/kg over 15-20 min; else maintence
fluids.
 1st dose of antibiotic, correct hypoglycaemia/
dyselectrolytemia if present

26. Monitor for features of resolution of shock/fluid
overload: HR,CRT,peripheral temperature, BP, Urine
output, sensorium,gallop rhythm,liver span, RR, basal
creptations.
20min: Therapeutic goals Therapeutic goals NOT
attained attained
Continue monitoring

27. Therapeutic goals not attained
No signs of fluid Signs of fluid overload
Fluid bolus 10-20ml/kg to cumulative
bolus of upto 40ml/kg.
Monitor for fluid overload
Therapeutic goals not attained
40min Start inotropes

28. Fluid refractory shock
 Reassess clinical status.
 Assess for remediable cause of shock:
Tamponade/Pneumothorax/Abdominal compartment
syndrome
 If possible monitor
 Invasive BP or
 Perform echocardiography( Cardiac Index, Stroke
index, Systemic vascular resistance index) or
 SCvO2 and
 Haemoglobin

29. Warm Shock Cold Shock
Prefer Norepinephrine Prefer Epinephrine
MAP below 5-50th centile Catecholamine
resistant shock
60min
Hydrocortisone 50mg/m2 after taking baseline sample for cortisol
Consider vasopressin
If cardiac dysfunction consider: Dobutamine, milrinone,levosimendon

30. Therapeutic endpoints of
resuscitation of septic shock
 Normalization of the heart rate
 Capillary refill of <2 seconds
 Well felt dorsal pedis pulses with no differential
between peripheral and central pulse
 Warm extremities
 Normal range of systolic pressure and pulse pressure
 Urine output > 1ml/kg/h
 Return to baseline mental, status, tone and posture
 Normal range respiratory rate
 Normal blood lactate and ScvO2>70%

31. Anaphylactic Shock
 Supplemental oxygen should be given.
 Intramuscular epinephrine is treatment of choice and
dose is 0.1 ml/kg of 1:10000 solution every 3-5 minutes
with max dose of 1 mg
 If hypotension is refractory to initial epinephrine
boluses, start epinephrine infusion at 0.1 mcg/kg/min
and may increase upto 1 mcg/kg/min

32. Obstructive shock management
 In obstructive shock definitive management depends
on underlying etiology.
 Cardiac tamponade- Aggressive volume expansion
can worsen the condition.
 Pericardiocentisis is the definitive treatment
Tension pneumothorax- immediate needle
thoractomy in the 2nd intercostal space in
midclavicular line at 90 degree angle using under
water seal.
Defenitive treatment is to insert chest tube to prevent
reaccumulation of free air

33.  Duct dependent congenital heart diseases-
Initition of intravenous infusion of prostaglandin E1
(0.05-0.2 mcg/kg/min)
 Balloon atrial septostomy
 Cardiology and cardiac surgery consultation for
definitive management
 Massive pulmonary embolism-Inotropic support
should be given.
 Fibrinolysis or thrombectomy in association with
cardiac intervention radiologist

34. Neurogenic Shock management
 Initiate supplemental oxygen support.
 Fluid resuscitation with crystalloids at the rate of
20ml/kg over 15-20 min and reassess.
 As there is loss of sympathetic drive, diffuse
vasodilation and decreased contractility develops
which needs inotropic support with norepinephrine
and or Epinephrine.
 Temperature fluctuations should be monitored.

35. Take Home Message
 Shock is a progressive process
 Shock is not equivalent to hypotension
 Goal of management is maintenance of perfusion and
oxygen delivary to the tissues.
 Early recognition, early aggressive appropriate
resuscitation
 Ongoing monitoring is of utmost importance for fluid
and vasoactive titration.

36. THANK YOU