This document provides an overview of shock in children, including: 1. Definitions of shock and the pathophysiology involving reduced tissue perfusion and oxygen delivery. 2. The epidemiology and classifications of different shock types, including hypovolemic, distributive, cardiogenic, and obstructive shock. 3. Details on the causes, signs, symptoms, and stages of specific shock types like septic, hemorrhagic, and cardiogenic shock. 4. The goals of evaluating and managing shock in children, including rapid assessment of appearance, breathing, circulation, history, and physical exam findings.

1. July 2019
Modulators: Dr.Dereje
Dr.Anteneh
Presenter:
Million Negasa( B
pharm)
1

2. 2
Out lines
 Definition
 Review of basic physiologic aspects
 Epidemiology of shock
 Pathophysiology
 Classification by type & severity
 Approach & Management
 References

3. SHOCK: Definition
• Shock is an acute process characterized by
the body’s inability to deliver adequate
oxygen to meet the metabolic demands of
vital organs and tissues.
– Significant reduction of systemic tissue perfusion,
resulting in decreased tissue oxygen delivery
3

4. 4

5. Physiology
Preload
Contractilit
y
Afterload
Cardiac
Output
Stroke
Volume
X
Heart rate
5

6. Oxygen Delivery
• Oxygen Delivery
=> Cardiac Output x Arterial Oxygen
Content
• Arterial Oxygen Content
=> Oxygen content of the RBC + the oxygen
dissolved in plasma
6

7. Epidemiology
• Shock occurs in approx. 2% of all hospitalized
infants, children, & adults in developed countries
• The mortality rate varies based on the
etiology and clinical circumstances.
• Mortality from shock is less among children than
adults. For children with severe sepsis, mortality is
about 10 %, in comparison to 35 to 40 % within
one month of the onset of septic shock for adults.
7

8. Epidem....
• Nevertheless, outcomes for children with
shock (in terms of morbidity & cost) are
significant.
• Hypovolemic shock, the most
common cause of shock in children
world wide
– Which is most frequently caused by
Diarrhoea, Vomiting, or Haemorrhage
8

9. Pathophysiology of Shock
9
The combination of a continued presence of an inciting trigger and
the body’s exaggerated and potentially harmful neurohumoral,
inflammatory, and cellular responses leads to the progression of
shock.

10. Types of Shock (Etiologically)
1. Hypovolemic shock
2. Distributive shock
a. Septic Shock
b. Anaphylactic Shock
c. Neurogenic Shock
3. Cardiogenic shock
4. Obstructive shock
10

11. Types of Shock
Type of
Shock
Pathophysiology Signs & Symptoms
Hypovolem
ic
↓PRELOAD: ↓CO,
↑SVR,
intravascular
volume loss
↑HR, ↓ pulses, delayed RF,
dry skin, sunken eyes, oliguria
Distributive ↓ AFTERLOAD
(SVR)
Anaphylacti
c
↑ CO, ↓SVR
Angioedema, low BP,
wheezing, respiratory distress
Spinal Normal CO, ↓SVR Low BP without tachycardia;
paralysis,
Septic Variable More to come
Cardiogenic ↓CO, Variable SVR Normal to ↑HR, ↓pulses, 11

12. 12

13. Cardiogenic Shock
Cardiac output falls due to the pathology in the
heart itself & is defined as CI < 2.2 L/min/m2.
• Cardiac Pump Failure 20
to poor myocardial function
• Manifested physiologically as systolic function & CO.
• Cardiogenic shock is uncommon among children than
adults
• Diverse mechanisms can be divided into 3 general categories:
1. Cardiomyopathies
2. Arrhythmias : Structural Heart Disease,
Drug Intoxications, and Hypothermia are
leading causes of arrhythmia in children
3. Obstructive disorders
13

14. Distributive Shock: causes
• Is a state of abnormal vasodilatation & decreased SVR.
 Abnormal Vessel Tone (decreased after load)
 Sepsis: gram-negative sepsis, other infections
 Anaphylaxis
 Neurogenesis (Spinal)
 Spinal cord transection
 Anesthesia
 Drug overdose
 Drug intoxication (Diuretics), hypoxia, poisoning
14

15. Septic
Shock
Decrease
d Volume
Decreased
Pump
Function
Abnormal
Vessel
Tone
15
Septic Shock =Severe sepsis plusplus the persistence of
hypoperfusion or hypotension despite adequate fluid
resuscitation or a requirement for vasoactive agents
Sepsis is the most common aetiology of distributive
shock among children

16. Obstructive Shock: Causes
16
Impaired diastolic filling
( Ventricular Preload).

17. HYPOVOLEMIC SHOCK: Causes
Hemorrhagic :
External
hemorrhage:
• Trauma
• Hematoma
Internal
Hemorrhage:
• GIT Bleeding
• Hemothorax /
Hemoperitoneum
Non-Hemorrhagic
External:
– Vomiting, Diarrhea, DHN
– Polyuria
– Burns
Internal (third spacing):
– Pancreatitis
– Bowel obstruction
– Ascites
17

18. Hemorrhagic Shock classification by
Severity
• Four classes based upon % loss of blood volume.
• As with nonhemorrhagic losses, clinical features
are typically used to estimate BV deficit.
• Many children with class II hemorrhage, and
• All of those with classes III & IV are in shock.
18

19. Hemorrhage Severity Classification
19
Classe
s
% of fluid
Loss
Symptomss/Signs Treatment
I Up to 15% Minimal physiologic changes are evident Crstalloid fluid
II 15-30% Mild tachycardia & tachypnea with a
narrow PP, slightly DCR, decreased
UOP, & mild anxiety.
Crstalloid fluid
May require Blood
products
III 30-40% Tachycardia, Tachypnea,
Hypotension, DCR, Altered
Mentation, Oliguria
Crstalloid solution &
Most Pt Need Blood
IV >40% Usually cold & pale with profoundly
depressed mentation, marked tachypnea
& tachycardia, and anuria.
Quick Blood products
Operative Intervention
often necessary to
control haemorrhage

20. Hypovolemic Shock
Clinical symptoms
• Often manifests initially as orthostatic
hypotension and is associated with
 Dry mucous membrane, dry axillae
 Sunken fontanel/eyes
 Poor skin turgor
 DCR, Cool extremities
 Low or no urine output
• Tachycardia => compensated shock!
• Normal BP until volume loss >30-40%
• Further volume loss and exacerbation of shock by
pre-existing low plasma oncotic pressure 20

21. • Hypotension is typically a late finding among
children in shock.
• For children, hypotension is defined as a
systolic blood pressure < 5th
percentile of
normal for age:
– < 60 mmHg in term neonates
– < 70 mmHg in infants
– < 70 mmHg + 2x age in years in 1 to 10
years
– < 90 mmHg in children >10 years of age
21

22. C/M ... General
• Regardless of etiology, in uncompensated shock,
late in the progression of disease:
– Hypotension
– High SVR
– Decreased cardiac output
– Respiratory failure
– Obtundation, and
– Oliguria
– Elevated blood lactate levels
• Reflect poor tissue oxygen delivery in all forms of
shock. 22

23. • Additional clinical findings in shock include:
– Cutaneous lesions such as
• Petechiae
• Diffuse erythema
• Ecchymoses
• Ecthyma gangrenosum and
• Peripheral gangrene
23

24. Shock – Effects on Organ
 Heart – CO / hypotension / myocardial depressants↓
 Lung - gas exchange / tachypnoea/ pulmonary edema↓
 Endocrine – ADH reabsorption of water→ ↑
 CNS – perfusion – drowsy↓
 Blood - Coagulation abnormalities – DIC
 Renal - GFR - urine output↓ ↓
 GIT – mucosal ischaemia – bleeding & hepatic enzyme↑
levels
24

25. Compensatory Mechanism
 Baroreceptors and Chemoreceptors- Disinhibits
vasomotor centers which increases adrenergic
output.
 Renin-Angiotension system- Angiotensin I and
Angiotensin II
 Antidiuretic Hormone/Vasopressin
 Adrenal Cortex- Aldosterone
 ACTH from pituitary- Cortisol
25

26. Stages of Shock
Compensated Shock
Decompensated Shock
Irreversible Shock
26

27. 1. Compensated (Nonprogressive) Shock
• Compensatory mechanisms attempts to
maintain BP: NORMAL BP
• Unexplained tachycardia
• Mild tachypnea
• Delayed capillary refill
• Orthostatic changes in pressure or pulse
• Irritability
27

28. 2. Decompensated (Progressive) Shock
 It is a state of inadequate end-organ perfusion
 Compensatory mechanisms fails & HYPOTENSION
occurs.
 Increased tachycardia, increased tachypnea
 Altered mental state, low urine output,
 Poor peripheral pulses.
 Capillary refill markedly delayed
 Cool extremities
28

29. 29

30. 3. Irreversible (Refractory) shock
• It occurs as a consequence of decompensated
shock not managed properly and at right time.
• Permanent cellular damage & MODS.
• Recovery does not occur even with adequate
restoration of circulatory volume
• Death occurs due to:
– Refractory Acidosis, Myocardial & Brain
Ischemia.
30

31. Complications of Shock
The main complications of severe shock
are:
1. Shock Lung (ARDS)
2. Acute Renal Failure
3. Gastrointestinal Ulceration
4. Disseminated Intravascular Coagulation
5. Multisystem Organ Failure
6. Death
31

32. Approaches to Shock
Patient
32

33. Goals of the initial Evaluation of
Shock
Immediate identification of life-threatening
conditions.
(eg, tension pneumothorax, hemothorax, cardiac
tamponade, or pulmonary embolism).
Rapid recognition of circulatory compromise.
Early classification of the type and cause of shock.

34. Rapid Assessment

35. Appearance
 Significant changes in appearance
like:
poor tone
unfocused gaze indicators of decreased cerebral
perfusion.
weak cry
Subtle differences in appearance
decreased responsiveness to caretakers & painful
procedures.

36. Breathing
A child with depressed mental status as the result
of shock may not be able to maintain a patent
airway.
 Tachypnea without respiratory distress can
develop in response to metabolic acidosis.
Children with cardiogenic shock typically have
some increased work of breathing in addition to
tachypnea.

37. Circulation
 Quality of central and peripheral pulses
 Decreased intensity of distal pulses in comparison to
central pulses suggests peripheral vasoconstriction and
compensated shock.
 Bounding pulses may be present in patients with
distributive (“warm”) shock.
 Skin temperature
 Skin may be mottled or cool in children with
compensated shock.
 This finding can also be influenced by environmental
temperature.

38. Con…
 Capillary refill
 >2seconds .
 Flash capillary refill (<1 second)
 The usefulness of capillary refill is limited by:
• inter-observer variability.
• environmental temperature.
Heart rate
 Tachycardia ( compensated shock )
 Bradycardia (Hypoxia, spinal cord injury and some
drugs).

39. History
1. Hx of injurey
2. A history of fluid loss
3. Fever and/or immunocompromised
4. A history of exposure to an allergen
5. Hx of exposure to toxins
6. Patients with chronic heart disease
7. risk for adrenal insufficiency

40. Approach to the classification of undifferentiated
shock in children, Does a child has…?

42. Physical Examination
V/S
•Abnormal V/S provide essential information regarding :
– Severity, classification & cause of shock.
A.RR –usually tachypneic.
B.HR
o sinus tachycardia (except cardiogenic shock from a
brady arrhythmia or spinal cord injury).
o In compensated shock, it may be the only abnormal
vital sign.
o Other causes of tachycardia with poor perfusion in
children include: (SVT & VT)

43. Con…
C. BP : normal / low BP.
D. T° : Fever (hypothermia in young infants)
E. Others: Stridor, wheezing (anaphylaxis).
C.Crackles (pneumonia, septic shock / HF, cardiogenic
shock).
D.Distended neck veins (HF, or cardiac tamponade or
tension pneumonia- or hemothorax).
E.Abnormal heart sounds ( murmurs or a gallop rhythm
/ muffled heart tones
F.Pulse differential
G.Hepatomegaly

44. Con..

45. Con…

46. DX
A. clinically (hx & p/e ).
E.g

47. Con…
B. Laboratory findings
i. comprehensive metabolic panel (CMP)
RBS ?
arterial or venous blood gas analysis
blood lactate
serum electrolytes ( Na+, K+, Ca++...)
BUN and SCr
ionized blood calcium
STB & ALT

48. Con…
II. Complete Blood Count
Hb
WBC differential (Neutropenia & leukopenia are
ominous sign of overwhelming sepsis).
III. Coagulation studies
thrombocytopenia may herald a bleeding disorder.
Disordered coagulation cascade activation
(Prolonged PT & aPTT , INR, Low Fibrinogen
and D-dimer)
IV. Culture body fluids( blood, urine, CSE..)

49. Con…
VI. Others
U/A ,Diagnostic serologic testing .
Inflammatory biomarkers (eg, C-reactive
protein).
B. Imaging
I.Chest x-ray.
II.Echocardiography
III.Catheterization and angiography

50. RX SHOCK

51. Shock Management Principles
1. Supportive Care
– ABC of Life
– Intubation, mechanical ventilation, Oxygen as
needed
1. Fluid Management
2. Treatment of underlying causes
51

52. Initial Management
• Early recognition and prompt intervention are
extremely important in the management of all
forms of shock.
• Regardless of the cause: ABC Don’t Ever Forget
Glucose
• Baseline mortality is much lower in pediatric
shock than in adult shock i.e due to early
interventions.

53. key steps to manage shock
1. Give oxygen (for infants 0.5 -1 l/min, older children 1-
2 l/min).
2. Give 10% Glucose 5 ml/kg by IV.
3.Keep the child warm.
4.Direct manual pressure to control
bleeding.
5. Take blood samples for emergency laboratory tests
6. Give IV fluids
7. First assess the child for severe malnutrition before
selecting treatment.

54. Intravenous Fluids
A. Shock With NO SAM
Fluid bolus of 20ml/kg isotonic fluid (maximum of 3X)
 If there is still NO improvement:
Consider Blood Transfusion unless there is profuse
watery diarrhea.
In this case, repeat Ringer's lactate.
 If shock remains refractory following 60-80 mL/kg of
volume resuscitation, vasopressor therapy (norepinephrine,
or epinephrine) .

55. B. Child With SAM
• The severely malnourished child is considered to have
shock if he/she is lethargic or unconscious and has
cold hands plus either:
– slow capillary refill (>3seconds), or
– weak, fast or absent radial or femoral pulses and
– absence of signs of heart failure in an edematous child.

56. Con…
 Weight a child.
 IV Fluid (15ml/kg over 1hr).
 Give normal saline or Ringer lactate with 5% glucose.
 check PR and RR every 5-10 minutes.
 If improved, change the IV fluid with oral intake/
Resomal after 2 hr.
 If there is improvement: Repeat 15ml/kg over 1 hr.

57. Con…
If there is NO improvement:
 Call senior health worker.
 Give maintenance IV fluid 4ml/kg/hr while
waiting for blood.
 Transfuse fresh whole blood at 10ml/kg slowly
over 3 hrs.
 use packed cells, if in cardiac failure.

58. Con…
 Monitor with the Multi-chart and shock follow up chart.
 Use one of the following solutions, listed in order of
preference:
 Ringer’s lactate solution with 5% glucose*
 0.9 per cent normal saline with 5% glucose*
(add 125 ml of 40 % or 100 ml of 50% glucose to 1
liter of 0.9% saline to make this fluid)
 *If either of these are used, add sterile potassium chloride
(20 Mmol/l) if possible.
 Observe the child and check RR and PR every 10 minutes.

59. Con…
• If the RR (by 5 BPM) and PR (by 25 PPM) increase and child is
gaining weight.
– stop the IV rehydration & assume septic or cardiogenic
shock.
• If RR & PR are slower after 1hour, the child is improving.
– Repeat the same amount of IV fluids for another hour.
– Continue to check RR & PR every 10 minutes.
• After two hours of IV fluids, switch to oral or NG rehydration with
ReSoMal.
• Give 5-10 ml/kg ReSoMal in alternate hrs. with F-75 for up to 10
hrs or until fully rehydrated.

60. A- HYPOVOLEMIC SHOCK
TREATMENT
GOAL – restore circulating volume and tissue
perfusion & correct the cause
1. Assess airway.
2. Administer oxygen.
3. Give IV Fluid bolus of 20ml/kg isotonic fluid
(maximum of 3) .
In case of shock refractory to fluids, start inotrope
(dopamine).

61. B- septic shock
Provide broad-spectrum antimicrobial agents.
 Neonates (ampicillin plus cefotaxime and/or
gentamicin).
intraabdominal process is suspected, anaerobic
coverage ,such as metronidazole, clindamycin, or
piperacillin-tazobactam.
Nosocomial sepsis ( 3rd- or 4th-generation
cephalosporin or a penicillin with an extended
Gramnegative spectrum). e.g., piperacillin-tazobactam.

62. Con…
community-acquired infections with Neisseria
meningitidis (3rd-generation cephalosporin,
(ceftriaxone or cefotaxime)).
resistant Streptococcus pneumoniae & MRSA require
the addition of vancomycin.
immunocompromised patients (Empirical coverage for
fungal infections).

63. C- Distributive shock
primary abnormality in vascular tone.
may benefit temporarily from volume
resuscitation.
early initiation of a vasoconstrictive agent to
increase SVR .

64. con…
1. ANAPHYLACTIC SHOCK
Airway, Withdrawal of Ag, Cautious fluid
administration
IV epinephrine
Antihistamine
Corticosteroids
Vasopressors or Inotropes

65. Con…
2. NEUROGENIC SHOCK
Cautious fluid administration
Vasopressors & Inotropes
Correct hypothermia
Treat bradycardia with atropine
Observe and prevent DVT.
•May benefit from :phenylephrine or vasopressin
to increase SVR.

66. D- cardiogenic shock RX
GOAL :
increase CO, treat reversible causes& decrease myocardial
workload
1. Assess airway , administer oxygen /mechanical ventilation
2. Inotropic agents, vasoactive drugs.
3. IV fluids (5-10ml/kg boluses over longer time)
4. Morphine to decrease preload and anxiety
5. Short acting beta blockers for refractory tachycardia

67. E- obstructive shock
• fluid resuscitation may be briefly temporizing in
maintaining cardiac output.
• primary insult must be immediately addressed.
Such as…
– pericardiocentesis for pericardial effusion,
– pleurocentesis for pneumothorax
– thrombectomy/thrombolysis for PE.
– prostaglandin infusion for ductus-dependent
cardiac lesions.

69. Dopamine
 Low-dose: 1 to 5 mcg/kg/minute, results in increased renal blood
flow and urine output
 Intermediate-dose: 5 to 10 mcg/kg/minute, results in increased
renal blood flow, heart rate, cardiac contractility, and cardiac output
 High-dose: >10 mcg/kg/minute, alpha-adrenergic effects begin to
predominate, resulting in vasoconstriction, increased blood pressure
in addition to increased heart rate, cardiac contractility, and cardiac
output due to beta-adrenergic effects.

71. Physiologic indicators and target goals
After the initial fluid bolus, evaluate for:
1) Quality of central and peripheral pulses (strong,
distal pulses equal to central pulses)
2) Skin perfusion (warm, with capillary refill <2
seconds)
3) Mental status (normal mental status)
4) Urine output (≥1 mL/kg per hr)
5) BP (systolic pressure at least fifth percentile for
age)

72. PROGNOSIS
 In septic shock, mortality rates are as low as 3% in
previously healthy children and 6-9% in children with
chronic illness (compared with 25-30% in adults).
 This is due to early recognition and therapy.
 But still shock and MODS remain one of the leading
causes of death in infants and children.
 The risk of death depends on:
 underlying etiology.
 presence of chronic illness.
 host immune response.
 timing of recognition and therapy.

73. References
1. NELSON TEXTBOOK OF PEDIATRICS 20TH
&
21th EDITION.
2. UPTODATE 2018.
3. PEDIATRIC HOSPITAL CARE: ETHIOPIA
(SECOND EDITION, 2016).
4. GUIDELINES FOR THE MANAGEMENT OF
ACUTE MALNUTRITION, FMOH, 2016.
73Shock Seminar: By Firomsa D &
G/Tsadik E

74. 74Shock Seminar: By Firomsa D &
G/Tsadik E