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MANAGEMENT OF SHOCK
General management of Shock
• Positioning
• Airway and breathing
• Vascular access
• Fluid resuscitation
• Monitoring
• Frequent reassessment
• Laboratory studies
• Medication therapy
• 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.
• 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.
• In obstructive shock 10-20ml/kg isotonic
crystalloid fluid may initially given to maintain
CO but rapid identification is needed for
effective management.
• Monitoring: Heart rate
Blood pressure
Temperature
Respiratory rate
O2 saturation by pulse oxymetry
Mental status
Urine output
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
PBF:
WBC- immature neutrophil,
vacuolation, toxic granules
 Prothrombin Time: ↑ , APTT:↑
Serum albumin: ↓
Serum fibrinogen: ↓
FDP: ↑
RBS: ↑ /↓
Serum electrolyte: Imbalance.
Serum Calcium: ↓
ABG: metabolic acidosis (pH↓), high anion gap.
-PaO2 ↓
Serum lactate: ↑
Renal Function Test: Serum Creatinine- N/ ↑
X-ray chest P/A view: ARDS
Need to exclude pneumothorax, pericardia
effusion
Cardiovascular Drug treatment of Shock
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;
Drug Effect Dosing range Comment
Dopamine
↑ Cardiac
contractility
3-20 Âľg/kg/min
↑ Risk of arrhythmias
at high doses
Significant
peripheral
vasoconstriction at
>10 Âľg/kg/min
Epinephrine
↑ Heart rate and ↑
cardiac
contractility
0.05-
3.0 Âľg/kg/min
May ↓ renal perfusion
at high doses
Potent
vasoconstrictor
↑ Myocardial
O2 consumption
Risk of arrhythmia at
high doses
Drug Effect(s) Dosing range Comment(s)
Dobutamine
↑ Cardiac
contractility
1-10 µg/kg/min —
Peripheral
vasodilator
Norepinephrine
Potent
vasoconstriction
0.05-
1.5 Âľg/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 Âľg/kg/min
Can cause sudden
hypertension
↑ O2 consumption
HYPOVOLEMIC SHOCK
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
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).
• 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 >10Âľgm/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-.
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.
CARDIOGENIC SHOCK
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.
• 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.
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)
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
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
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
SEPTIC SHOCK
• Septic shock is most common and caused by
infectious organism or their by-product (eg,
endotoxin).
Septic shock
Hypovolumic
shock
Cardiogenic
shock
Distributive
shock
Intravascular
fluid losses
through capillary
leaks
Myocardial
depressant
effects of sepsis
↓ systemic
vascular
resistance
Alteration of preload, afterload &
myocardial contractility
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
PATHOPHYSIOLOGY OF SEPTIC
PROCESS
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
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.
• 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.
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.
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
TH
36

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seminar on Management of shock

  • 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
  • 8. PBF: WBC- immature neutrophil, vacuolation, toxic granules  Prothrombin Time: ↑ , APTT:↑ Serum albumin: ↓ Serum fibrinogen: ↓ FDP: ↑ RBS: ↑ /↓
  • 9. Serum electrolyte: Imbalance. Serum Calcium: ↓ ABG: metabolic acidosis (pH↓), high anion gap. -PaO2 ↓ Serum lactate: ↑ Renal Function Test: Serum Creatinine- N/ ↑ X-ray chest P/A view: ARDS Need to exclude pneumothorax, pericardia effusion
  • 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 Âľg/kg/min ↑ Risk of arrhythmias at high doses Significant peripheral vasoconstriction at >10 Âľg/kg/min Epinephrine ↑ Heart rate and ↑ cardiac contractility 0.05- 3.0 Âľg/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 Âľg/kg/min — Peripheral vasodilator Norepinephrine Potent vasoconstriction 0.05- 1.5 Âľg/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 Âľg/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 >10Âľgm/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).
  • 27. Septic shock Hypovolumic shock Cardiogenic shock Distributive shock Intravascular fluid losses through capillary leaks Myocardial depressant effects of sepsis ↓ systemic vascular resistance Alteration of preload, afterload & myocardial contractility
  • 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
  • 36. TH 36