This document provides an overview of shock in pediatrics, including epidemiology, classification, pathogenesis, clinical manifestations, and principles of management. It begins with an introduction defining shock and its causes. It then discusses the main types of shock - hypovolemic, cardiogenic, distributive, and septic shock. The document reviews the epidemiology of shock in developing countries and the United States. It also provides details on the pathophysiology, clinical features, diagnosis, and management approaches for different shock types. The goals of treatment are outlined as restoring circulatory volume and blood flow while monitoring the patient.

1. State Specialist Hospital Gombe (SSHG)
Department of Paediatrics
Dr. Ibrahim Adamu
22 March, 2022
Moderator: Dr Rukaiyya

2. OUTLINE
• Introduction
• Epidemiology
• Classification
• Pathogenesis
• Clinical manifestation
• Principles of Management
• Conclusion
• References
2

3. INTRODUCTION
• Shock is state of acute circulatory failure due to inadequate tissue
perfusion resulting in generalized cellular hypoxia
• It is a state of acute energy failure due to inadequate glucose and oxygen
delivery and/or mitochondrial failure at cellular level
• Body’s inability to to meet up with metabolic
demands of the body
3

4. INTRODUCTION
• The condition may arise from:
- Volume: Reduction in the total circulatory volume
- Vessel: Inappropriate volume distribution
- Pump: Heart pump failure
• The clinical state of shock is diagnosed based on vital signs, physical
examination and lab data
4

5. INTRODUCTION
• Delay in recognition, initially compensated
• Continued presence of inciting agent + body’s exaggerated response
Lead to progression of shock
If untreated Irreversible tissue injury
Irreversible shock
5

6. EPIDEMIOLOGY
• The incidence of shock vary around the world by country and by age
• Shock is one of the leading cause of death in developing countries.
Why so?
• In 2018, 2.6 million neonates died of shock worldwide and 5.8 million
death among children aged 1-59 months
• In the U.S shock accounts of 37% of paediatric referral to tertiary
centers with sepsis been the leading cause of shock (57%) followed by
hypovolaemic shock (24%), distributive shock (14%) and cardiogenic
shock (5%)
6

7. EPIDEMIOLOGY
• In Kenya, shock accounts for 24.5% of paediatric presentation to the
emergency with septic shock accounting for 12.5% and mortality of
70% in 72 hours
• Out of 554 acutely ill children, 79% were found to have shock in a
study at UBTH, Nigeria.
• 38.3% develop shock while still on admission
7

8. CLASSIFICATION
• Hypovolaemic
• Cardiogenic
• Distributive
• Septic
8

9. HYPOVOLEMIC SHOCK
• Reduction in circulatory volume characterized by fluid loss
• Can be hemorrhagic
• Non-hemorrhagic
a. Loss of plasma as occurs in extensive bums or peritonitis
b. Loss of ECF as occurs in diarrhea, vomiting
9

10. CARDIOGENIC SHOCK
leading to reduced cardiac ouput
• It is commonly due to myocardial infarction, cardiomyopaties, CHD,
arrhythmias, contussion, tamponade, myocarditis etc
10

11. DISTRIBUTIVE SHOCK
• Caused by
Capillary leak
• Maldistribution of fluid into interstitium
• Neurogenic as seen in Post spinal cord or brainstem injury
• Anaphylaxis as seen in penicillin, anesthetics, stings, venom
• Poisonings
11

12. SEPTIC SHOCK
• Complex interaction of distributive, cardiogenic and hypovolemic shock
• Due to bacterial, viral or protozoal infections which release toxins
leading to shock
• Gram + septic shock is due exotoxin release from bacteria like C. tetani,
Staphylococcus, Streptococcus, Pneumococci etc
• Gram - bacteria causes endotoxaemia
SIRS Sepsis Severe Sepsis Septic Shock
12

13. PATHOPHYSIOLOGY
• O2 consumption in the body is 3mls/kg/min=200-250mls for an average
adult
• O2 delivery from arterial blood is 1000mls/min , i.e its 5 times O2
consumption
• If the ration falls to less 2:1 , then tissue hypoxia leading to shock
• Oxygen delivery to tissues depend on
Aerobic metabolism is not maintained due to hypo perfusion.
13

14. PATHOPHYSIOLOGY
14

15. STAGES OF SHOCK
Compensated Shock
a. Constriction of veins
b. Increased heart rate
c. Redistribution of blood to vital organs
d. Compensation of metabolic acidosis
e. Maintenance of intravascular volume
NB: BP and urine output is normal
15

16. STAGES OF SHOCK
is - Uncompensated
- Marked Tachycarida or Bradycardia
- Tachypnoea with acidosis
- Oliguria/Anuria
- Altered mental status
- Hypotension
< mo: 60mmHg, 1mo to 10y = Lower limit of SBP = 70 + (2 x age in years)
>10 yr: 90mmHg
16

17. EFFECTS OF SHOCK
• Heart: Decreased cardiac output and hypotension
• Lung: Interstitial oedema leads ARDS
• Metabolic: anaerobic metabolism leading to lactic acidosis
• Cellular changes:- due to release of lysosomal enzymes causing cell death
• Brain:- perfusion, when decreases the patient becomes drowsy and comatose
• Kidney : GFR decreases and tubular reabsorption of salt and water increases but in
severe cases tubular necrosis sets in
• Blood: Alteration in cellular components including platelets leads to DIC. It causes
bleeding from all organs.
• Gastrointestinal tract: Mucosal ischemia develops causing bleeding from GIT with
hematemesis and melena. It is aggravated by DIC.
17

18. CLINICAL FEATURES
- May be conscious, confused, restless, apathetic
- or comatose
- Skin mottling
- Cold and clammy extremities
- Delayed capillary refill
- Mucous membrane is pale and cyanotic
Septic shock: The skin initially may be warm and flushed because of peripheral vasodilation
18

19. CLINICAL FEATURES
- Rapid, weak and thready pulse
- Low or unrecordable blood pressure
- Rapid and deep respiration (air hunger)
- Tachypnoea
- Oliguria or anuria and severe thirst
19

20. CLINICAL FEATURES
• In
• Pulmonary edema may develop with respiratory distress, crackles
raised JVP and hepatomegaly
• In Pericardial effusion they may be muffled heart sounds with
distended neck veins
• In P.E they may be hx of acute chest pain and symptoms of right sided
heart failure, gallop rythm, cyanosis and hypotension
20

21. CLINICAL FEATURES
• In
• There is subnormal temperature with warm extremities and bounding
peripheral pulse
Septic shock is a medical emergency that requires prompt and efficient resuscitation. If possible
patient should be admitted to ICU
21

22. DIAGNOSIS
• Through history and physical examination
• Lab findings
- : Increased FDP, PT, PTT
- : electrolyte imbalances, Sr lactate, SrCr, BUN
- : leucocytosis/leucopenia, thrombocytopenia and anemia
- : cardiomegaly, bat-wing sign, hyperinfation
- Blood culture, Sputum m/c/s, Urine m/c/s, Wound
swab m/c/s, Endocervical swab m/c/s or any exudate. Based on
suspected source; CXR, Abd-Xray, Abd-pelvic USS
22

23. PRINCIPLES OF MANAGEMENT
1. Resuscitation
2. Restoration of blood volume and specific treatment
3. Monitoring
23

24. RESUSCITATION
24

25. RESTORATION OF CIRCULATORY VOLUME
Fluid bolus of of isotonic fluid (N/S or R/L) is started
over 30-45min, then reassess the PR, BP, urine output. If still deranged,
repeat fluid (maximum of 3) otherwise consider septic shock in non-
hemorrhagic shock
• An exception to repetitive volume resuscitation is child with cardiogenic
shock
in severe blood loss, crystalloid shows only transient improvement.
25

26. RESTORATION OF CIRCULATORY VOLUME
in absence of blood, colloids; human albumin, fresh
frozen plasma, dextran 10 or 70, haemacel, gelofusine
after adequate fluid therapy but perfusion remains
inadequate (fluid refractory shock); Dopamine and epinephrine for
Patient in cold shock while norepinephrine is recommended in warm
shock
for patients with catecholamine-resistant shock despite
adequate volume, blood and electrolytes
26

27. Drugs used in shock
- Inotrope at low dose 1-5 mcg/kg/min
- Peripheral vasocontriction at >5-15 mcg/kg/min
- Arrythmia at higher doses
- Useful in distributive shock
- Increase caridac contractility
- Peripheral vasodilator
- 1-10mcg/kg/min
- Useful in cardiogenic shock
27

28. Drugs used in shock
- Increase HR and cardiac contractility
- Potent vasoconstrictor
- 0.05-3 mcg/kg/min
- Potent vasoconstrictor
- No significant effect on caridac contractility
- 0.05-1.5mcg/kg/min
28

29. Drugs used in shock
- Potent vasoconstrictor
- 0.5-2 mcg/kg/min
- Vasodilator (mainly arterial)
- 0.5-4 ug/kg/min
29

30. Drugs used in shock
- Vasodilator (mainly venous)
- 1.0-2.0 ug/kg/min
- Increase cardiac contractility and peripheral vasodilation
- 0.5-1 ug/kg/min
30

31. Management of cardiogenic shock
to increase contractility
to decrease afterload
• Cautious (5-10ml/kg may be administered)
to decrease preload and anxiety
• Short acting Beta blockers for refractory tachycardia
• Pericardial drainage for effusion
• Anticoagulants or thrombolectomy for P.E
Goal is to improve C.O and decrease cardiac workload
31

32. Management of anaphylactic shock
• Identification of trigger
• Antihistamines
• Corticosteroids
• Vasopressor or inotropes
• Cautious fluid administration
32

33. Management of septic shock
Norepinephrine – 1st line for septic shock refractory to
volume replacement.
In a cleared and patent airway, O2 is delivered via a face mask
to increase O2 saturation.
•
33

34. Management of septic shock
: should be commenced early.
• Empirical IV Broad spectrum and bactericidal & anerobe coverage
• For Septic shock of unknown origin
- Gentamicin
- 3rd generation cephalosporin
- Vancomycin for resistant staphylococci or enterococci
- Metronidazole especially for abdominal sources
34

35. Management of septic shock
superoxide dismutase, allopurinol, vitamin C
has been found to ↓morbidity/mortality
Recombinant human activated
protein C
e.g debridement, drainage of abscess
35

36. 36

37. MONITORING
• Vital signs: Pulse and Blood pressure
• Intake and output balance
• Temperature control
• Urine output
• Clinical signs of depletion or overload
• Electrolytes & RBS
• Absolute rest, analgesics to relieve pain
• Blood gases
PO2 maintained between 80-100mmHg. If PO2 falls below 60mmHg and the PCO2 rises above
45mmHg, then ventilatory support is necessary
37

38. CAUSES OF DEATH IN SHOCK
1. Pulmonary insufficiency
2. Cardiac failure/arrest
3. Cerebral failure
4. AKI
5. Metabolic acidosis
6. Sepsis/SIRS
7. Liver Failure
8. Failure of coagulation and immune systems.
9. Multiple organ dysfunction syndrome
38

39. CONCLUSION
• Shock remains an important cause of morbidity and mortality despite
advances in technology and pathophysiological understanding
• Initial priority is aimed at the general principles of resuscitation
• The goal of therapy is to restore adequate tissue perfusion
39

40. REFERENCES
•Jonathan C. Azubuilke, Kanu E. Nkanginieme, Paediatrics and Child
Health in a Tropical Region 3rd edition
• Nelson Textbook of Paediatrics 19th Edition
• Robert M. Kliegman, Bonita F. Stanton, Joseph W. St. Geme III, Nina
F. Schor, & Richard E. Behrman Pediatric Textbook 4th Edition
• Website: http://www.emedicine/medscape.com/shock578763.
Accessed on Saturday, 20th March, 2019, 3:36pm
40

41. THANK YOU
FOR
LISTENING
41