8. pediatric shock management and classification MD3.ppt

pediatric shock management and classification MD3.ppt

1. PATHOPHYSIOLOGY PATHOPHYSIOLOGY
AND AND
MANAGEMENT OF MANAGEMENT OF
SHOCKSHOCK
Presenter: Dr Tatu S. Mbotoni

2. Presentation Outline
Introduction
Pathophysiology
Management

3. Introduction

4. Definition of shock
An acute, dramatic syndrome of circulatory
collapse characterized by:

Inadequate tissue perfusion
Poor O2 supply
Poor waste removal

Anaerobic metabolism
Lactic Acidosis

5. When a patient is in shock, one or more
of the three parts is not working properly.

6. Anaerobic Metabolism
InadequateInadequate
CellularCellular
OxygenationOxygenation
AnaerobicAnaerobic
MetabolismMetabolism
MetabolicMetabolic
FailureFailure
MetabolicMetabolic
AcidosisAcidosis
InadequateInadequate
EnergyEnergy
ProductionProduction
Lactic AcidLactic Acid
ProductionProduction
Cell Death!Cell Death!

7. Pathophysiology

8. Causes of Shock

9. Classification of the causes of shock

10. Other classifications
Absolute hypovolemia

emesis, diarrhea, trauma,
peritonitis
Functional hypovolemia
vascular capacity
increases ie. spinal cord injury,
anaphylaxis
cold shock
predominance of Vasoconstriction.
warm shock
predominant vasodilation
Hyperdynamic
Increased CO, decreased SVR
Hypodynamic
Decreased CO, Increased SVR

11. What happens?
The pathophysiologic pathway to cardiovascular failure
results from impairment of the two components of BP:
cardiac output (CO)
systemic vascular resistance (SVR)
Initial insult (Causes) triggers shock which disrupts
perfusion to end organs.
CO (HR & SV) is affected by:
ventricular filling (preload)
The impedance to ventricular ejection (afterload)
Intrinsic pump function (myocardial contractility).
OR BOTH

12. Compensatory mechanisms in Shock
Aim:
Maintain BP, thus Perfusion to vital organs
They include:
Increased HR, SV, SVR tone (Progressive Vasoconstriction)
RR (increase CO2 excretion)
Increased renal excretion of H+ and bicarbonate retention
Decreased Urine output
Maintenance of vascular volume is facilitated by:
RAAS and atrial natriuretic factor (thru Na+ regulation)
Cortisol and Catecholamine Synthesis and Release
Secretion of ADH

13. Renin-Angiotensin-Aldosterone
PlasmaPlasma
volumevolume
 [Na+][Na+]
KidneyKidney
(juxtaglomerular(juxtaglomerular
apparatus)apparatus)
Detected by
Releases
ReninRenin
Angiotensinogen
Angiotensin I…
Converts
&/Or
Via ACE
(Angiotensin
Converting
Enzyme)
Angiotensin II…

14. Renin-Angiotensin-Aldosterone
Angiotensin II…
 vasoconstriction  PVR
 BP!
 thirst
Fluid
volume
ADH
(anti-diuretic
hormone))
Adrenal
cortex
Releases
Aldosterone
Na+
reabsorption

15. In Children…
BP maintenance depends on
CO & SVR
CO is more dependent on HR
than on SV
Tachycardia is thus the child’s
principal means of maintaining
an adequate CO
Children maximize SVR to
maintain a normal BP, even with
significant decreases in CO.
BP = CO X SVR
CO = SV X HRCO = SV X HR
Note…
SHOCK CAN & DOES EXIST WITHOUT HYPOTENSION!!

16. Thus…
The evaluation of the following are more
valuable than BP in child’s circulatory status
heart rate
end-organ perfusion
capillary refill
the quality of the peripheral pulses
mentation
urine output
acid-base status

17. Clinical progression and
stages of shock
Shock is a progressive disorder
The progression may be:
fulminant as in massive hemorrhage
evolving over a span of hours
This progression has been arbitrarily
divided into 2 stages.
1)
     Early shock (compensated)
2)
     Progressive shock (decompensated)

18. Early (compensated)
 shock
Vital organs perfusion &
functions are maintained
by compensatory
mechanisms
Presentation

Blood pressure is usually
maintained
HR (usually the 1
st
Sign)
pulse pressure is narrow

cold extremities
prolonged CFT

19. Decompensated Shock
Defense mechanisms begin to fail

Failure of Tx of compensated shock
Presentation
Hypotension (Usually late presentation)
Prolonged Cap refill time (CRT) with poor urinary output
Marked increase in heart rate
Rapid, thready or absent peripheral pulse
Laboured and irregular breathing
Agitation, restlessness, confusion

20. Irreversible Shock
Complete failure of compensatory
mechanisms
Multisystem organ Dysfunction
Death even in presence of resuscitation

21. Hypovolemic Shock
Type of shock due to decrease of circulating
(Intravascular) volume
Most common type of shock in children
Classified as
Hemorrhagic (Blood loss)
Nonhemorrhagic (Plasma loss)
Water loss from vomiting and diarrhea most common
cause

22. Common Causes of Hypovolemic
Shock in Children

23. Diarrhea and vomiting
Children suffering hypovolemic shock due to fluid and
electrolyte losses have both intravascular and interstitial
depletion.
Clinical findings include:
Poor urine output
Sunken eyes & anterior fontanelle
dry mucous membranes
poor skin turgor
delayed capillary refill
cool extremities.
Cardinal
features of
dehydration

24. Burn injury
Patients afflicted with hypovolemic shock due to increased
capillary permeability, eg burns, have
Intravascular hypovolemia in the setting of interstitial euvolemia
or hypervolemia.
Their clinical presentation tends to be dominated by signs
of decreased end-organ perfusion:

mental status changes

decreased urine output

cool, but often swollen, distal extremities.
They do not exhibit classic signs of dehydration.

25. Once again, hypotension is a late finding and
may not occur until intravascular volume has
decreased by 30% to 40%, reflecting failure
of the child’s compensatory increase in
heart rate and SVR.

26. Septic Shock
It is a combination of
 
Distributive shock – decreased SVR
Cardiogenic shock – myocardial depressant effects of
sepsis

hypovolemic shock – Intravascular fluid losses occur
through capillary leak.

27. Septic Shock: Definitions
Systemic Inflammatory response syndrome (SIRS):
Presence of at least 2 of the following 4 criteria, 1 of
which must be abnormal temperature or WBC.
Core Temperature,
Tachycardia
Mean respiratory rate
abnormal WBC.
Infection: suspected or proven infection caused by any
pathogen or a clinical syndrome associated with high
probability of infection.

28. Definitions Cont…
Sepsis: SIRS in the presence of suspected or proven
infection.
Severe Sepsis: Sepsis + 1 of the following;
Cardiovascular organ dysfunction or
ARDS or
2 or more other organ dysfunctions (Renal, hepatic, hematologic,
Neurologic)
Septic Shock: sepsis and cardiovascular organ
dysfunction.

29. Inflammatory Mediators
Proinflammaroty
mediators

Tumor necrotic factor

Interleukin-1

Interleukin-6

Interleukin-8

Interleukin gamma
Anti infammatory
mediators

Interleukin-1

Interleukin-1

Soluble Receptor and
Receptor Antagonist

30. Cardiogenic Shock
Cardiogenic shock in children usually result from
impaired myocardial
 dysrhythmias
Redirected blood flow caused by congenital heart
lesions may impair myocardial contractility
Congenital heart defects that present with shock are
those with left ventricular outflow tract obstruction
Coarctation of aorta
Congenital Aortic Stenosis

31. Distributive Shock
Distributive shock occurs because of a loss of SVR
Extensive vasodilatation results in abnormal distribution
of blood flow within the microcirculation – functional
hypovolemia.
Cardiac contractility is increased initially
CO is also compromised due to lack of preload.
Main Causes
Sepsis (Septic Shock)
Anaphylaxis (Anaphylactic Shock)
Spinal cord injury (neurogenic shock)

32. Anaphylactic shock
Anaphylactic shock is an immediate,
life-threatening systemic reaction to an allergic stimulus
food, medication, bee sting
immunoglobulin E-mediated hypersensitivity response
massive release of cytokines from mast cells and
basophils.
Patients usually have

respiratory distress from angioedema

hypotension

hypoperfusion caused by rapid loss of vascular tone

third-spacing of intravascular volume.

33. Symptoms and signs of
Anaphylaxis

34. Neurogenic Shock
Rare and usually transient disorder that follows an acute
injury to the spinal cord.
The clinical presentation results from the generalized
loss of sympathetic vascular and autonomic tone.
Cardiac contractility usually is preserved
CO may eventually be compromised due to the lack of
venous return and preload.
Physical examination reveals hypotension in
the absence of tachycardia.

35. Management

36. Investigations
Blood:
serum electrolytes, BUN,RBG, ABG/CBG,
coagulation Indices, LFT, Inflammatory markers
Urine:
Urinalysis
Chest X – ray and ECG
Sepsis workout:
CBC, Blood C/S, CSF C/S, urine C/S

37. Primary Assessment of the patient

Assess Airway patency
by the “look, listen, and
feel” method.
Assess the adequacy of
Breathing

Effort of breathing
Recession
Respiratory rate
Grunting
Accessory muscle use
Flare of the alae nasi
Efficacy of breathing
Breath sounds
Chest expansion/abdominal
excursion
Effects of breathing
Heart rate
Skin colour
Mental status
Assess the adequacy of
Circulation.

38. Cardiovascular status
Heart rate
Bradycardia in a shocked child is caused by hypoxia and
acidosis and is a preterminal sign.
Pulse volume
generally poor pulse volume
In early septic shock – high output state which will produce
bounding pulses.
Capillary refill
Blood pressure

A formula for calculating normal systolic blood pressure is:
70 + (2 x Age in years)

39. Effects of circulatory inadequacy
on other organs
Acidotic sighing respirations
rapid, deep breathing.
Pallor, cyanosis or cold skin
A core/toe temperature difference of more than 2°C is a
sign of poor skin perfusion.
Mental status
Agitation or depressed conscious level.
Urinary output

40. Look for the presence of signs of
heart failure
Tachycardia
Raised JVP (often not seen in infants in heart failure)
Lung crepitations on auscultation
Gallop rhythm
Enlarged liver

Lastly, listen for a heart murmur.

41. Assess for Disability
Assess neurological function.
The AVPU scale

A – ALERT

V – responds to VOICE

P – responds to PAIN

U – UNRESPONSIVE
Pupillary size and reaction should be noted.
Note the child’s posture
children in shock are usually hypotonic.
Note any convulsive movements

42. Assess for Exposure
Take the child’s core and toe temperatures.
Look for a rash
if one is present, ascertain if it is purpuric.
Look for evidence of poisoning.

43. ‘10’ Key Features from Clinical
Assessement of a child with Shock

44. Resuscitation
Airway:
A patent airway is the first requisite.
Breathing:

All children in shock should receive 100% oxygen
(4l/min) through a face mask, nasal catheter or
nasal prong as soon as the airway is patent.

If the child is hypoventilating, respiratory support is
warranted.

45. Circulation
Gain intravenous or intraosseous access
 Take blood for FBC, U&Es, blood culture, cross-match,
glucose stick test and laboratory test
 Give 20 ml/kg rapid bolus of crystalloid to all patients
except for those with signs that heart failure is their
primary pathology.

0.9%NS, RL or 5% albumin if available

½ strength NS or RL+ 5%Dextrose if hypoglycemic
Remember 3Tubes

46. Hypovolemic Shock
Fluids given rapidly as boluses of 20ml/kg of
N.Saline / R.Lactate.
Reassess - if signs of shock persist multiple
boluses are given often upto 40-60ml/ kg.
Generally a child with hypovolemic shock
responds to 2-3 boluses.
If hemorrhagic, Whole blood 20mg/kg

47. Cardiogenic Shock
Pts usually have N or intravascular volume.
bolus NS 10ml / kg over 20minutes should be given
monitor liver span and signs of fluid overload.
If signs of fluid overload, stop fluids and start inotrops
CVP monitoring is very essential
Vasoactive drugs
Dopamine is indicated when blood pressure is low
dobutamine is preferred when the blood pressure is normal or high.

48. Septic Shock
aggressive volume replacement
Some children may require fluids up to 200ml/kg in the first
hour
Continuous monitoring of the HR, RR, peripheral perfusion,
BP, MS and urine output
Stop IV fluids, start dopamine infusion even with persistent
shock and intubate when

span or work of breathing increases

fresh rales appear or gallop rhythm occurs
hypoglycemia and hypocalcemia should be corrected
promptly

49. Antibiotics in Septic Shock
Broad spectrum bactericidal antimicrobials
should be administered when sepsis is
suspected
cefotaxime/ceftriaxone + aminogycoside/
vancomycin

50. Anaphylactic shock
treated with fluid and vasopressor resuscitation
antihistamines and steroids
may slow the release of mediators and help reverse
symptoms.
The offending agent should be sought and
further exposure prevented

52. Cardiogenic Shock
Tx of cardiogenic shock consists of
pharmacologic support of CO
volume resuscitation
Ductal Dependent CHD
PGE1 (alprostadil) 0.05-0.2microgram/kg/min
Intubation & inotropic support

53. Other forms of shock
Obstructive Shock
Surgical release of the Obstruction etc

54. Vasoactive and steroid therapy
Children with fluid refractory shock, require vasoactive
support
dopamine is the first line drug started at 10- 15µgm/ kg/
minute at 15 minutes.
Dopamine and dobutamine resistant shock

epinephrine for cold shock

noradrenaline for warm shock
In catecholamine resistant shock, consider adrenal
insufficiency,

hydrocortisone 2mg/kg as a bolus followed by 2mg/kg infusion over
24 hours

55. Vasoactive medication Cont…
All shock states, some form of impairment of
 
myocardial function
vasoactive therapy to optimize CO is therefore the
cornerstone of shock therapy.
They should be used after volume resuscitation has
been done.

56. Inotropes
drugs which improve myocardial contractility
Effective in cardiogenic and fluid refractory shock.
Dopamine: 

most commonly used vasoactive agent

recommended as the first line agent in fluid refractory septic shock and
for hypotension after resuscitation from cardiac arrest.

Dobutamine : 
preferred in cardiogenic shock
selective stimulant of β1 receptors.

normotensive/ hypertensive shock

57. Inotropes Cont…
Adrenaline:

preferred in post arrest shock states

cardiogenic shock not responding to dobutamine

septic shock
Noradrenaline:

warm septic shock
its µ - adrenergic effect

spinal shock

anaphylaxis.

58. Vasoactive/Cardiotonic AgentsDopamine
1-5 mcg/kg/min: dopaminergic
5-15 mcg/kg/min: more beta-1
10-20 mcg/kg/min: more alpha-1
may be useful in distributive shock
Dobutamine
2.5-15 mcg/kg/min: mostly beta-1, some beta-2
may be useful in cardiogenic shock
Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2
> 0.1 to 0.2 mcg/kg/min: alpha-1

59. Correct Metabolic Abnormalities
Acidosis:

if the base defect is more than 6 meq/L

Correct with 8.4%sodium bicarbonate 1-2mEq/kg
Hypocalcemia 

can impair the myocardial function

Correct with
CaCl2 10% 10-20mg/kg
Ca gluconate 100mg/kg in 10 -15min
Hypoglycemia 
is very common in shock states
Electrolyte abnormalities

60. Hyponatremia and hypernatremia
Mild & Moderate Hyponatremia:
0.9% NS or RL
Severe Hyponatremia:
3% NaCl 12mg/kg (6mmol/kg)

Hypernatremia:

Corrected slowly (48hrs) to avoid cerebral oedema.

Desmopressin (DDAVP) 1.25microgram/day or BD

61. Potassium and Calcium Disturbances
Mild and Moderate Hypokalemia:
Oral KCl 1 – 4mEq/kg/day, bd or qid
Severe Hypokalemia:

IV KCl 7.5% 0.1 – 0.5mmol/kg hr in 3hrs by infusion
pump

If there is Metabolic Acidosis (HCO3 < 28mmol/L or
Anion gap <12): Give NaHCO3 1ml/kg (8.4%), 2ml/kg
(4.2%) or 4ml/kg(1.4%)
Note: Correction of Hypokalemia takes up to 6wks
NEVER GIVE POTASSIUM IV BOLUS

62. Hyperkalemia
Hyperkalemia: - Give the following Sequentially:
1.IV CaCl 10%0.1 – 0.3ml/kg (Max 5ml) or Ca gluconate
10% 0.5ml/kg in 10min
2.NaHCO3 7.5%1-2mmol/kg IV (for older children)
3.Glucose 0.5 – 1g/kg in insulin 1.0U/gm of Glucose in 1hr
4.Furosemide 1mg/kg IV
5.Nb infants <2years use NaHco3 4.2% solution
Initial :1meq/kg/min over 1-2 min THEN 0.5mEq/kg IV
over 10 min. (not to exceed 8mEq/kg/day)

64. Respiratory rate
ACIDOSIS LEADS TACHYPNEA
Age dependent
<2m 60
≤
<11m 50
≤
≥1yr 40
≤
≥3yrs 30
≤

65. age Systolic Pressure
(mm/Hg)
0-1 m 60
1m-1 yr 70
>1 yr 70 + (2 x age in yrs)
Diastolic pressure = more o less 2/3 of systolic
pressure
Normal blood pressure for age

66. References
Paediatrics Acute patients Care Guideline, Department of pediatrics, NMH
(Nov, 2007)
Nelson Textbook of Pediatrics, 18
th
Edition
Oxford Handbook of Pediatrics
Dr.Lalitha
 Kailas, shock in
Children Clinical%20paediatrics/Shock%20in
%20Children.htm
Handbook of Pediatric Emergence medicine
Advance Pediatric Life Support, The Practical approach, 3
rd
edition, BMJ
McKiernan et al, Circulatory Shock in Children: An Overview
Dr. Ed Snyder et al, Department of Surgery, Huntington Memorial Hospital:
shock
www.blearning.com, Shock: chapter 10.