2. General management of Shock
• Positioning
• Airway and breathing
• Vascular access
• Fluid resuscitation
• Monitoring
• Frequent reassessment
• Laboratory studies
• Medication therapy
3. • Positioning: If hemodynamically stable ,
allow the child remain in most comfortable
position.
If the child is hypotensive and breathing is
compromised : Trendelenburg position.
• Airway and Breathing: High concentration of
O2 supplementation has to be given to all
patients with shock.
If respiration is ineffective, mental status is
impaired or work of breathing is significantly
increased => need O2 with ventilation.
4. • Fluid resuscitation: Infusion of 20ml/kg
bolus isotonic crystalloid solution over
5-20 min → can be given upto 3 bolus at a
time over 60 min (In all types of shock except
cardiogenic and obstructive shock)
• In cardiogenic shock: Infusion of 5-10ml/kg
bolus isotonic crystalloid solution over 10-
20min→ given to maintain initial CO but if
patient is deteriorating ,stop infusion
immediately and manage accordingly.
5. • In obstructive shock 10-20ml/kg isotonic
crystalloid fluid may initially given to maintain
CO but rapid identification is needed for
effective management.
6. • Monitoring: Heart rate
Blood pressure
Temperature
Respiratory rate
O2 saturation by pulse oxymetry
Mental status
Urine output
7. CBC
Hb%- ↓
TC-WBC: ↑ or ↓ (ominous sign of sepsis)
DC-WBC: Neutrophil- shifted to left ( immature
form ↑ - bands, myelocyte, promyelocyte).
Neutrophil ↓ (ominous sign)
ESR- ↑
CRP: ↑
Platelet count: ↓
Investigation
11. Medication Therapy
DRUGS INDICATION
DOPAMINE Given in all types of shock
Preferred fluid refractory septic
shock as a vasoactive agent
DOBUTAMINE Given with dopamine if only
dopamine use is not beneficial
Typically used in cardiogenic
shock, septic shock
ADRENALINE •Preferred vasoactive agent in
“cold shock” as it increases stroke
volume
•Treatment of choice for
anaphylactic shock
NORADRENALIN
E
Combination with dobutamine
may be used in septic shock;
12. Drug Effect Dosing range Comment
Dopamine
↑ Cardiac
contractility
3-20 µg/kg/min
↑ Risk of arrhythmias
at high doses
Significant
peripheral
vasoconstriction at
>10 µg/kg/min
Epinephrine
↑ Heart rate and ↑
cardiac
contractility
0.05-
3.0 µg/kg/min
May ↓ renal perfusion
at high doses
Potent
vasoconstrictor
↑ Myocardial
O2 consumption
Risk of arrhythmia at
high doses
13. Drug Effect(s) Dosing range Comment(s)
Dobutamine
↑ Cardiac
contractility
1-10 µg/kg/min —
Peripheral
vasodilator
Norepinephrine
Potent
vasoconstriction
0.05-
1.5 µg/kg/min
↑ Blood pressure
secondary to ↑
systemic vascular
resistance
No significant
effect on cardiac
contractility
↑ Left ventricular
afterload
Phenylephrine
Potent
vasoconstriction
0.5-2.0 µg/kg/min
Can cause sudden
hypertension
↑ O2 consumption
15. Management of Hypovolemic Shock
Mainstay of Management - Fluid resuscitation
• Identification of type of volume loss (non-
hemorrhagic /hemorrhagic)
• Replacement of volume deficit
• Prevention and replacement of ongoing loss
• Restoration acid –base balance
• Correction of metabolic derangement
16. Stepwise management of Hypovolemic
Shock
• Infusion of 20ml/kg bolus isotonic crystalloid
solution with in 20 min→ can be given upto 3
bolus at a time over 1 hour
• If there is hemorrhage 3 bolus of crystalloid
solution 20ml/kg is needed and for blood
replacement 10ml/kg PRBC or 20ml/kg whole
blood (transfusion given in significant blood loss
and crystalloid refractory hemorrhagic shock).
17. • Medication Therapy: Vasoactive agents are not
routinely indicated for hypovolemic shock
management. Given in case of
-Morbid child with profound hypovolemic shock
-Hypotension
Inj. Dopamine >10µgm/kg/min
• Acid- Base balance: Both respiratory alkalosis and
metabolic acidosis occur in hypovolemic shock.
But alkalosis couldn’t completely compensate.
Bicarbonate is indicated if there is significant loss
of HCO3-.
18. Obstructive shock
• Treatment of underlying cause
-pericardial drain, chest tube, surgical
intervention
-if the patient is a neonate with a ductal
dependent lesion then give PGE
• Further evaluation, invasive monitoring,
pharmacologic therapy, appropriate
consultation to be done according to cause.
20. TREATMENT
• Treatment is aimed at reinstitution of
adequate cardiac output and peripheral
perfusion
• Slow adminstration (10-20 min) fluid bolus
(5-10 ml/kg bolus ) with careful monitoring
for response.
• Management of underlying cause.
21. • Administration of ionotropes
Dopamine is the 1st line agent.
Milrinone improves systolic function and
decreases SVR without a significant increase in heart
rate. Also causes diastolic relaxation.
Dobutamine & other vesodilator may be
considered.
Epinephrine- in pt with persistant, profound
hypotension.
22. Cont...
• Pt with deteriorating cardiogenic shock may get
benefit from
-Left ventricular assist device(LVAD)
- Right and left ventricular assist
device(BiVAD)
- Extracorporeal membrane
oxygenation(ECMO)
23. Distributive Shock
• It is characterized by high CO and low SVR
(opposite of hypovolemic, cardiogenic, and
obstructive)
• Maldistribution of blood flow causing inadequate
tissue perfusion
• Due to release of endotoxin, vasoactive
substances, complement cascade activation, and
microcirculation thrombosis
• Early septic shock is the most common form
24. Management of Anaphylactic Shock
• Specific treatment: Inj.Adrenaline I/M 0.01mg/kg
repeat the second dose after 10 to 15 minutes in
severe anaphylaxis
• Salbutamol nebulization for bronchospasm
• Antihistamines: Diphenhydramine
• I/V Corticosteroid
25. Management of Neurogenic Shock
• Treatment- initial fluid therapy.
• Phenylephrine and vasopressin causes
vasoconstriction and may be considered in the
treatment for pt with spinal cord injury
26. SEPTIC SHOCK
• Septic shock is most common and caused by
infectious organism or their by-product (eg,
endotoxin).
28. CAUSATIVE ORGANISM
In neonate -- Group B strept
Escherichia coli
Listeria monocytogenes
enterovirus
herpes simplex virus
In older children
Streptococcus pneumoniae
Neisseria meningitidis
Staph aureus (methicillin sens or resistant)
In immunocompromised and hospitalized pt-
Escherichia coli,
pseudomonas
klebsiella,
Acinetobacter
Enterobacter
Serratia
30. Focus of infection
Superantigens and
endotoxin
Activated inflammatory cell Activation of host defence
Endogenous mediator release
Pro-inflammatory cytokines
Anti-inflammatory cytokines
Platelet activating factors
Arachidonic acid metabolite
Myocardial depressant substance
Endogenous opiates
Activation of
coagulation system
Activation of
complement system
Activated endothelium-increased
expression of endo derived adhesion
molecule
Decreased thrombomodulin, increased
plasminogen activator inhibitor
Thrombosis and antifibrinolysis
Hypovolemia, cardiac and vascular failure,
capillary leak, ARDS, DIC, decreased steroid
synthesis
SHOCK MODS
DEATH
31. Septic shock has 2 phases:
• Early or Warm shock- occurs in some patients with
- increased hyperdynamic cardiac output and
- decreased systemic vascular resistance.
- manifested by bounding pulse, widened pulse
pressure
• Late or Cold shock- occurs in other patients with
-decreased cardiac output
-elevated systemic vascular resistance.
-manifested by poor peripheral perfusion(prolonged
capillary refill)
In both cases ,perfusion to major organ systems may be
compromised.
32. • Antibiotic therapy
• Anemia should be treated in the setting of septic shock
to improve delivery of oxygen to the tissues. Most
experts recommend maintaining a hemoglobin level 10
g/dL (hematocrit of 0.30 [30%]) in the setting of septic
shock.
• Treatment of hypoglycaemia and hypocalcemia
• Identification and correction of metabolic
derangement.
33. Treatment outline
Proper counselling.
ABC management.
Fluid therapy.
Use of vasoactive drugs.
Correction of metabolic abnormality.
Use of antibiotics.
Adjuvent therapy.
Treatment of cause.
Follow up and monitoring.
34.
35. TAKE HOME MESSAGE
• Goal of therapy is identification, evaluation, and treatment of
shock in its earliest stage
• Initial priorities are for the ABC’s
• Fluid resuscitation begins with 20cc/kg of crystalloid or
10cc/kg of colloid
• Subsequent treatment depends on the etiology of shock and
the patient’s hemodynamic condition
• Successful resuscitation depends on early and judicious
intervention
• Aggressive resuscitation except if cardiogenic