The document provides information on pediatric shock, including: 1) It defines shock and discusses its pathophysiology, classification, signs, and goals of management. Shock results from inadequate tissue perfusion and can be classified as distributive, hypovolemic, cardiogenic, obstructive, or septic. 2) Early recognition of shock is important as children can deteriorate rapidly. Signs include altered mental status, prolonged capillary refill, diminished pulses, and low urine output. 3) Management involves stabilizing the airway, providing oxygenation and ventilation, restoring circulating volume with fluid boluses, treating hypoglycemia, and using vasoactive drugs if needed to improve perfusion.

1. Paediatric
Shock
Dr. Hrishabh Soni
DNB pediatrics resident

2. 01
Defination of shock
Classification
03
Recognition
Physiologic
principles of shock
04
Management
Learning objectives
05
02

3. Shock is a clinical state characterized by inadequate tissue perfusion resulting in
delivery of oxygen and metabolic substrates that is insufficient to meet
metabolic demands.
Untreated: Multiorgan dysfunction and death
INTRODUCTION

4. Children often show few signs of shock even
after severe fluid depletion due to high
physiological reserves. This also means that
when symptoms do occur, patients are likely
to deteriorate rapidly.

5. Cold vs warm shock

6. A. Cardiogenic shock
B. Third spacing
C. Rebound anaphylaxis
D. Fluid overload
E. Hypercapnia
A 12-year-old child has been stung by a bee and has
developed an anaphylactic reaction. He has been given IM
adrenaline and his breathing has improved. However, his
hands, face and feet are now very swollen and his blood
pressure is still low.
What is pathophysiological mechanism causing this?

7. Many inflammatory mediators are released in anaphylaxis
causing vasodilation and increased permeability of
capillaries (they become more leaky). Fluid leaves the
capillaries and moves into the interstitial space, leaving
less fluid in the blood vessels. This results in a reduced
circulating volume which reduces blood pressure. The
blood pressure is also reduced due to the vasodilation
reducing systemic vascular resistance.
Answer - B

8.  Shock is one of the most common life threatening
presentations in paediatrics and accounts for 2% of
all paediatric admissions to casualty worldwide.
 Around 10 million children die of shock annually
worldwide. The highest mortality is in under 5s in
developing countries.
 Sepsis is the cause in the majority of paediatric
cases (57%) and has a high mortality rate ranging
from 5% in developed countries to 35% in
developing countries
Epidemiology

9. Early/Compensated
• Neurohormonal compensatory mechanisms maintain perfusion
pressure (SBP: Normal)
• It’s important to identify shock in this early stage itself.
Decompensated
• Compensatory mechanisms fail: Hypotension (SBP decreased)
• Requires and responds to therapeutic interventions
• Organ functions deteriorate
Irreversible or Refractory
• Irreversible organ injury: MODS
Classification Based on High or Low Blood
Pressure

10. When shock begins to develop, the body
uses neural and hormonal mechanisms to compensate
and increase blood pressure (BP) to perfuse the vital
organs. This state is called compensated shock and BP
is maintained .

11.  Tachycardia to increase cardiac output.
 Redistribution of blood flow to increase perfusion of more important organs at
the expense of others (e.g. skin) through a combination of vasodilation and
vasoconstriction.
 Tachypnoea to reduce anaerobic respiration and reduce lactic acidosis.
If the cause of shock is not treated, these mechanisms will become
insufficient to maintain BP and therefore, vital organ perfusion. This state
is called uncompensated or decompensated shock and is a bad prognostic
sign.
Mechanisms used in compensated shock
include:

12. CO = HR X SV
MAP = CO X SVR
SV: Preload, after load and contractility
Frank-Starling Phenomenon
In the normal heart, the diastolic volume (preload) is the principle force that
governs the strength of ventricular contraction
Physiologic Principles

13. Contractility
 Strength and efficiency of muscle contraction
 Influenced by metabolic state of myocardium and factors which
increase contractility
Afterload
 Sum of forces that oppose or impede ventricular ejection
 Approximated by the systemic or pulmonary vascular resistance
Contractility and Afterload

14. • HR & MAP can be easily measured at the
patient’s bedside.
MAP = DP+1/3 (PP)
• SV can be estimated by assessing peripheral
pulse volume and end organ perfusion (such
as urine output & GCS).
• SVR can be estimated by assessing
peripheral temperature and capillary refill
time.

15. A. Send home and encourage oral fluids
B. Give some oral antibiotics and reassure
C. Tell the mother to take the child to hospital for treatment
D. Call the hospital yourself and arrange an immediate ambulance transfer to the
A 4-month old child presents to your clinic with a non-blanching rash
present for a day. For the past 2 days he has also been crying more but over
the last few hours have now become more drowsy.
What is the best management option?

16.  Hypovolemic: Decreased preload
 Cardiogenic: Myocardial pump failure
 Distributive: Impaired vasomotor tone
 Obstructive: Increased afterload
 Septic: Predominantly distributive (Cardiogenic +
Hypovolemic)
Classification

17. A. Hypovolemic shock
B. Septic shock
C. Cardiogenic shock
D. Neurogenic shock
A 5-year-old patient with a recent urologic surgery comes into hospital
looking very unwell. His assessment reveals the following vital signs: blood
pressure 79/52, heart rate 142, temperature 39.2C. On exam you find
delayed capillary refill and weaker peripheral pulses compared to central.
What type of shock are you MOST suspicious of?

18. Septic shock
This is the most likely scenario. Key findings include fever, hypotension and delayed capillary refill.
Hypovolemic shock
This type of shock is unlikely without a history of trauma or a diarrheal-like illness.
Cardiogenic shock:
This type of shock is unlikely as a first presentation in a child of this age. However, in a case such as
myocarditis, hypotension, tachycardia and a fever may be found. In fulminant heart failure, one may also
see signs of systemic congestion, including hepatomegaly, however this is not always found. Therefore,
this type of shock should be included on the differential, but less likely when compared to septic shock.
Neurogenic shock
This type of shock is unlikely without a history of trauma or other reason for CNS involvement.You
would also not expect to find a fever.

19. Distributive
shock
01

20. This is a result of redistribution of a normal intravascular blood volume in the wrong
vessels due to systemic vasodilation.
Ordinarily, there is a degree of sympathetic tone in all vessels to allow dilation and
constriction depending on local circumstances; for example sending more blood to
the skin for temperature control, or the muscles during exercise, at the expense of
other areas. However, when all these vessels dilate simultaneously, it leads to shifts
of blood flow within the vascular system, resulting in reduced blood flow to major
organs despite a normal blood volume.
Systemic vasodilation is commonly caused by sepsis due to the release of many
inflammatory cytokines in response to infection, but can also be caused by
anaphylaxis or high spinal cord injury.
Distributive shock

21. Hypovolaemic
shock
02

22. Hypovolaemic shock
Reduced circulating blood volume decreases cardiac output
through Starling’s law, decreasing perfusion of the major organs causing
shock.
It is commonly caused by:
• Dehydration e.g. diarrhoea, vomiting, burns, inadequate feeding in
infants, or diuresis in diabetic ketoacidosis.
• Third spacing – the movement of fluid from the intravascular
compartment to an extracellular compartment i.e. the interstitial space.
In both sepsis and anaphylaxis, the release of inflammatory
mediators increases the permeability of capillaries, leading to fluid in the
capillaries moving to the interstitial space. One more example of similar
phenomenon is dengue shock.
• Hemorrhage.

23. Cardiogenic
shock
03

24. Cardiogenic shock
When the heart itself fails, this decreases the cardiac output, resulting in
reduced perfusion of the major organs. It should be suspected in a patient
who is not responding to fluid therapy and BP remains low and/or is
demonstrating signs of pulmonary overload (tachypnoea, respiratory
distress, hepatomegaly).
In paediatric patients, cardiogenic shock is commonly caused by viral
myocarditis, or acute deterioration of heart failure secondary to
cardiomyopathies or congenital heart defects.
This has a poor prognosis. Approximately a third of these children either die
or require a heart transplant within a year.

25. Obstructive
shock
04

26. Obstructive shock
An obstruction to the outflow of blood from the heart itself or the great
vessels decreases cardiac output and therefore perfusion of the major
organs.
This the least common cause of shock in paediatrics but can be caused by
coarctation of the aorta, cardiac tamponade, tension pneumothorax or
massive pulmonary embolism.

27. Differential diagnosis
Distributive Hypovolaemic Cardiogenic Obstructive
Sepsis Dehydration Myocarditis Tamponade
Anaphylaxis Third spacing Cardiomyopathy Pulmonary Embolism
High spinal injury Bleeding Arrhythmias
Tension
pneumothorax
Sepsis
Congenital heart
disease
Coarctation of the
aorta

28. Recognition of Shock
• Initial hours following diagnosis of shock: GOLDEN HOURS
• Interventions during golden hours: Higher survival rates and decreased organ
dysfunction.

29. Early Signs:
Any child with hypo/hyperthermia with signs of poor perfusion
• Altered mental status (anxiety, restlessness, seizure, or loss of
consciousness)
• Prolonged capillary refill time of >2 s or flash capillary refill
• Diminished or bounding peripheral pulses
• Mottled cool extremities
• Decreased urine output of <1 mL/kg/h

30. Late signs:
 Weak central pulses
 Altered sensorium
 Hypotension is a late sign and the child may rapidly
progress to cardiac arrest after hypotension sets in.

32. Systolic BP used for diagnosis
PALS (Pediatric Advanced Life Support) (1-10 years):
SBP = Age x 2 + 70.
>10 year - 90 mm Hg
Mean BP: Better indicator of tissue perfusion
• Not affected by cuff size, artery chosen
Diastolic BP
• Required for coronary perfusion
• Minimum diastolic desirable: >25% of systolic BP

33. Investigations
Shock often presents as an emergency and should be treated clinically. Do not
wait for investigations before beginning treatment. However, investigations
can be useful for assessing the severity of shock, the cause, and to
monitor improvement.
• Lactate and blood gases (lactic acidosis indicating ischaemia, and hypoxia).
• Creatinine to look for acute kidney injury (a sign of uncompensated shock).
• electrolytes to assess any electrolyte imbalances e.g. due to diarrhoea, and
guide IV fluid management.
Other investigations are guided by the suspected cause e.g. CBC, CRP,
coagulation profile, blood cultures

34. Management

35. Principles of Management
 Optimize perfusion and tissue oxygenation
 Oxygen and/or mechanical ventilation
 Fluids
 Vasoactive medications
 Correction of metabolic disturbances
 Supportive care
 Monitoring during and after resuscitation

36. Therapeutic End Points
• Normalization of the heart rate
• Capillary refill of ≤2 s
• Good pulse volume with no differential between peripheral and
central pulses
• Warm extremities
• Normal range of systolic pressure and pulse pressure
• Urine output >1 mL/kg/h
• Return to baseline mental status tone and posture
• Normal respiratory rate
• Normal blood lactate and Scvo2, ≥70%

37. Initial management :
An A to E assessment should be performed on all unstable patients.
Early identification of the type of shock present, is important to
guide management.
Airway and Breathing Circulation Disability Exposure
Effort of breathing Heart rate Conscious level Fever
Respiratory rateand rhythm Pulse volume Posture Rash
Stridor / wheeze Capillary refill Pupils Bruising
Auscultation Skin temperature
Skin colour

38. Initial stabilization and resuscitation:
In this phase, one must ensure increased oxygen delivery to tissues and
reduce oxygen demand. While managing the child if anaphylaxis is
suspected, switch to the anaphylaxis algorithm.
Within the first 10–15 minutes of detection of signs of shock, airway,
oxygenation, ventilation, and monitoring of heart rate/rhythm and pulse
oximetry should be taken care of and vascular access should be
established.

39. Factors Affecting Oxygen Delivery

40. Support airway and breathing:
Ensure effective oxygenation and ventilation, start high
concentration of oxygen preferably by high flow device
[nonrebreather mask (NRM)]. If the child is in respiratory
failure, ensure mechanical ventilation, continuous (SpO2)
monitoring and venous blood gas might help, look for
serum lactate level also.

41. Improving Preload: Choice of Fluids
• Able to achieve fast flow rate
• Easily available
• Low cost
• Ideally able to fill vascular compartment with minimum infusing volume
• Less side effects
• Should match physiological loss
Crystalloids: Saline, Ringer’s lactate-small molecules that move freely out of the
bloodstream
Colloid fluids: Plasma, albumin, dextrans, hetastarch large molecules with limited
movement out of the bloodstream (Matches albumin)
Red blood cells: Packed cells/Whole blood
(Standard resuscitation fluid is isotonic crystalloids (0.9% saline or Ringer’s
lactate or buffered crystalloids). Consider albumin and other colloids only in
case of albumin deficiency or large third spacing and blood products in
case of visible or occult blood loss.)

42. Fluid therapy in septic shock:
i. Start fluid therapy within the first 5 minutes of identification of shock in
the form of isotonic crystalloid solution as a 10–20 mL/kg bolus over
10–15 minutes. Reassess after every bolus and repeat fluid boluses if
needed to restore BP and perfusion.
ii. Total bolus fluid up to 40 mL/kg may be administered over the first
hour in hypotensive septic shock while starting maintenance fluids.
Do not give a bolus of fluids in the absence of hypotension. Keep
caution for pulmonary edema, especially in case of anemia and severe
febrile illness.

43. Glucose control:
Blood glucose ≤60 mg/dL is used to define
hypoglycemia (beyond the neonatal period).
Hypoglycemia should be identified rapidly and
corrected immediately. IV dextrose may be
administered as 25% dextrose (2 mL/kg), 10%
dextrose (5 mL/kg) or 5% dextrose (10 mL/kg).

44. Calcium and hypocalcemia:
Ionized hypocalcemia may impair cardiac performance and
should be corrected as it is common in neonates and children
with sepsis.

45. Bicarbonate therapy:
Do not use bicarbonate therapy for the purpose of improving
hemodynamics or reducing vasopressor requirements when
treating hypoperfusion-induced lactic acidemia with pH ≥ 7.15.

47. Improving Contractility
The pharmacologic agents may be classified as-
Inotropic medications, Vasopressors, and Vasodilators
 Inotropic medications increase cardiac output by increasing myocardial
contractility and/or heart rate
(Chronotropic: Increase heart rate
Lusotropic: Improve relaxation during diastole and decrease EDP in the ventricles)
Affecting Afterload
Vasopressors elevate SVR by increasing the tone of arterial circulation.
Vasodilators decrease arterial resistance, resulting in decreased afterload and
increased cardiac output without affecting contractility.

48. Vasoactive drugs: An appropriate vasoactive drug infusion should be
started if there is no response to fluid therapy:
i. Use epinephrine for cold shock, norepinephrine for warm shock, and
dopamine as an alternative (in both conditions).
ii. Vasoactive agents can be given through the peripheral line in
emergency setting. Try to shift to the central line as soon as possible
(restrict peripheral line vasoactive agent use to <6 hours). Vasoactive
agents when given through a peripheral line need to be diluted more.

49. Management
Algorithm

52. Cardiogenic Shock
Fluid resuscitation in cardiogenic shock should be guided by preload assessment and only in
presence of preload insufficiency (preferably by echocardiography)
• Small bolus of 5-10 mL/kg of bolus over 30 minutes to 1 hour
• In presence of fluid overload with ventricular dysfunction, loop diuretics (Furosemide)-
reach euvolemia
• Evidence for use of Tolvaptan/ Nesiritide - evolving

53. Hemorrhagic Shock
• Primary target is control of bleeding
• Hypotensive resuscitation: Targeting 5th centile BP-to prevent rebleeding
• Permissive hypotension: Restricting fluid administration-accepting brief period of
suboptimal end-organ perfusion.
• Hemostatic resuscitation:
• Early use of blood products rather than an abundance of crystalloids.
• Minimizes the metabolic derangement, resuscitation-induced coagulopathy, and the
hemodilution that occurs with crystalloid resuscitation.

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