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1. Shock

2. • Worldwide, shock is a leading cause of morbidity
and mortality in the pediatric population.
• Shock is defined as a state of acute energy failure
due to inadequate glucose substrate delivery,
oxygen delivery, or mitochondrial failure at the
cellular level.
• The clinical state of shock is diagnosed on the
basis of vital signs, physical examination, and
laboratory data, although its recognition in the
pediatric patient can be difficult.

3. • Delay in recognizing and quickly treating a state
of shock results in anaerobic metabolism, tissue
acidosis, and a progression from a compensated
reversible state to an irreversible state of cellular
and organ damage.
• Morbidity from shock may be widespread and
can include CNS failure, respiratory failure (ie,
from muscle fatigue or ARDS], renal failure,
hepatic dysfunction, gastrointestinal
ischemia, DIC, metabolic derangements, and
ultimately death.

4. • Shock is the most reversible causes of death in
children.
• An acute , complex state of circulatory
dysfunction that result in failure to deliver
sufficient amount of O2 and nutrient to meet
tissue metabolic demands
• Therefore, basically DO2< VO2
• If prolonged and left untreated- can lead to
multiple organ failure and eventually death.

5. • Oxygen delivery + cardiac output x atrial
oxygen content ( DO2+ COxCaO2)
• Cardiac output + HR x CO

6. • Shock is a physiologic state characterized by
systemic reduction in tissues perfusion,
resulting in decreased tissues oxygen delivery.

7. • It is a condition in which circulation fails to meet
the metabolic need of the tissue and at the same
time fails to remove the metabolic waste
products
• Inadequate tissue perfusion to meet demands
usually result of inadequate blood flow and or
oxygen delivery
• Inadequate peripheral perfusion leading to failure
of tissue oxygenation leads to anaerobic
metabolism

10. Compensatory Mechanism
SNS-adrenal response
- SNS- Neurohormonal response stimulated by
baroreceptors
• Increased heart rate
• Increased contractibility
• Vasoconstriction
• Increased preload

11. • SNS- hormonal: renin angiotensin system
• Decreased renal perfusion
• Release renin Angiotensin I
• Angiotensin II Potent vasoconstriction and
releases aldosterone adrenal cortex
• Water sodium retention( increased
intravascular volume)

12. • SNS-Hormonal :antidiuretic hormone
- Osmoreceptors in hypothalamus stimulated
- ADH released by pituitary
- Vasopressor effects to increase BP
- Acts on renal tubules to retain water

13. • SNS- Hormonal: adrenal cortex
- Anterior pituitary releases ACTH
- Stimulates adrenals to release glucocorticoids
- Blood sugar increases to meet increased
metabolic needs

14. Failure of compensatory responses
• Decreased blood flow to the tissues causes
cellular hypoxia
• Anaerobic metabolism begins
• Cell swelling, mitochondrial disruption, and
eventual cell death
• If low perfusion persist:
Death

15. Stages of shock
• Initial stage – tissues are under perfused,
decreased cardiac output, increased anaerobic
metabolism, lactic acid is building
• Compensatory stage- reversible. SNS activated by
low output, attempting to compensate for the
decrease tissue perfusion
• Progressive stage- falling compensatory
mechanism profound vasoconstriction from SNS
ischemic– lactic acid production is high
metabolic acidosis

16. Clinical presentation( Generalized
shock)
- Vital sign
• hypotension
• Tachycardia
• Tachypnea
- Mental Status
Irritability, restless, LOC, unresponsiveness
- Decreased urine output

17. Compensated
• Confusion
• Tachycardia
• Normal or mild tachypnea
• > CRT
• Urine out adequate
• BP normal

18. Uncompensated
• Drowsiness
• Marked tachycardia
• Tachypnea and acidosis
• Very slow CFT
• Oliguria/Anuria
• Hypotension

19. Irreversible
• Child is unresponsive
• Bradycardia
• Apnea
• Cold cyanotic skin
• Anuria
• Un-Recordable BP

20. • Hypotension formula
Ages- 1-10 years is defined as
<70 mm of hg +(age in years x2)mm of hg

21. Shock syndrome
• Hypovolemic shock
- Blood volume problem
• Cardiogenic shock
- Blood pump problems
• Distributive shock
- Blood vessels problem

22. Hypovolemic shock
• Loss of circulating volume “empty tank”
decrease tissue perfusio general shock
response
• Etiology
- Internal / external l fluid loss
- Intracellular/ extracellular compartments
• Most common cause
Hemorrhage and dehydration

23. External loss
• Fluid loss: dehydration
Nausea and vomiting, diarrhoea, massive
diuresis, extensive burns
• Blood loss
Trauma visible or invisible bleeding

24. Internal loss
• Loss of intravascular integrity
• Increased capillary membrane permeability
• Decreased colloidal osmotic pressure( third
spacing)

28. Presentation
• Tachycardia and tachypnea
• Weak, thready pulses
• Hypotension
• Skin cool and clammy
• Mental status changes
• Decreased urine output dark and
concentrated

29. Treatment
• Main goal- restore circulating volume and tissue
perfusion, correct the cause
1. Assess airway
2. Administer oxygen
3. Control bleeding and balance
4. Establish IV assess
5. Fluid boluses ( max-3) isotonic fluid
6. In case of shock refractory to fluids, start
inotrope(dopamine)

30. Cardiogenic shock
• The impaired ability of the heart to pump
blood
• Pump failure of the right or left ventricle
• Most common causes of MI

31. • When heart Is unable to contract and pump
blood efficiently due to inadequate supply of
O2 and nutrient to the heart

32. • Older age
• History of heart attack , heart failure
• CHD
• Hypertension
• Diabetic
• obesity

33. Etiological factor
• Acute MI
• Hypertension
• Cardiomyopathy
• Pericardial tamponade
• Acidosis dysrhythmias
• Trauma
• Structural abnormality
- Vulvur anomalies

37. Clinical manifestation
angina pectoris
Dysrhythmias
Diminished heart sound
Hypotension
Decreased cardiac output
SOB
Weak, thready pulse
decreased urine output
Cold clammy skin

38. Complication
• Brain damage
• Kidney damage
• Liver damage
• Multiple organ failure
• Coma
• Death

39. Management
• Correction of the underlying cause is important
to prevent
- Fail of the compensatory mechanism
- Reduces effectiveness of intervention
Correction of
- Dysrhythmias
- Acidosis, electrolyte imbalance:
-

40. • Initiation of 1st line treatment
- oxygenation-(2-6 lit)
- Hemodynamic monitoring
- Fluid balance
- Pain control

41. • Pharmacological management
- Dobutamine
- Dopamine
- Vasoactive medication
Epinephrine
Nor-epinephrine
vasopressin

42. • Surgical management
CBAG( coronary artery bypass graft)
Valve replacement

43. Distributive shock
• Inadequate perfusion of tissues through
misdistribution of blood flow
• Intravascular volume is mal-distributed
because of alterations in blood vessels
• Cardiac pump and blood volume are normal
but blood is not reaching the tissues

44. • Etiologies
- Septic shock (most common)
- Anaphylactic shock
- Neurogenic shock

45. Anaphylactic shock
• A type of distributive shock that result from
wide spread systemic allergic reaction to an
antigen
• The hypersensitive reaction is life threatening

46. • Anaphylaxis: reaction sudden life threatening
because the process immunologic of allergen-
antibody reaction
• Anaphylactic reaction causing physical the
same symptoms but caused no immunological
reaction

47. Stages of anaphylactic shock
• Changes in mast cell towards stimuli
• Activation of cell wall enzyme
• Meditators release
• Functional pathophysiology response
• Inflammation and release of secondary
meditators

48. Etiology
1) Associated with IgE
2) Non IgE
3) Causes of anaphylatoid
- Drugs like NSAID, antibiotics, alkaloids, food
additives

51. Clinical features
• Skin- itching erythema, urticaria
• Respiratory- sneezing runny nose, wheezing,
swollen larynx. Tightness, hoarseness, stridor,
cyanosis
• Digestive- nausea vomiting diarrhoea, abd
pain
• Eye- itching, tears
• Cardiovascular- collapse fainting, hypotension
pale, cold, tachycardia

52. Management
• Primary treatment
-Adrenaline 1:1000 with dose of 0.001ml/kg
maximum 0.3 ml SC
-Can be repeated 3 times
-head extended , ventilated position
-O2 2-3 lit

53. • Place patient in shock position
• Pulmonic resuscitation
• Oro-pharyngeal airway
• E insertion
• Tracheostomy
• Cardiac compression

54. Complementary treatment
• Intended for complication
- seizures- diazepam, phenobarbital, midazolam
- Bronchial spasm- Aminophylline 7mg with 10-
20 ml of 0.9& NaCl followed 9mg/kg/24
hours( divided into 3 dose)
- B-2 agonist: ventolin nebulizer

55. Additional
• Antihistamine
• H-2 receptor antagonist
• Corticosteroids

56. Septic Shock

57. • Septicemia is a condition when there is prolonged
presence of bacteria in the blood accompanied
by systemic reaction
• SIRS,I s a syndrome characterized by presence of
two or more of the following clinical criteria
- Temperature increased or decreased
- Tachycardia
- Respiratory rate >20b/m or PaCO2 <32 mm of hg
- Increased or decreased WBC

58. • Result from moderate to severe sepsis or
tissues damage. It is considered as part of a
spectrum and a progression of SIRS
• Sepsis: SIRS with a clearly established focus of
infection
• Septic Shock: refers to severe sepsis which is
not responsive to intravenous fluid infusion
for resuscitation and requires inotropic or
vasopressor agent to maintain SBP

59. • Multiple organ dysfunction (MODS)- altered
function of more than one organ system in an
actually ill patient requiring medical
intervention homeostasis.

60. • Epidemiology
-4.6cases/1000 in US
200,000 cases annually with 50% mortality
M>F
Leading cause in pediatric ICU

61. • Bacteria: gram negative nearly 2/3rd, gram
positive 1/3rd
• E.coli is commonest
• Gram negative

62. Source
Endogenous-
Skin
Urinary
Respiratory
Bowel
Exogenous-
surgical intervention
Drapes
Imaging machines
staff

63. Risk factors
• Age <10yr,<70yr
• Malnutrition
• Anemia
• Primary disease, malignancies, DM, CLD, CRF
• Necrotic issues
• Hematoma
• Poor surgical technique
• Catherization
• Prolong hospitalization
• Major surgeries

64. Pathogenesis
• Microorganism or product of tissue damage
stimulate production of pro-inflammatory
cytokines, which in turn stimulate production of
secondary mediators of inflammation
• The production of the pro-inflammatory
cytokines is regulated to limit damage
• However poorly control sepsis or extensive tissue
damage, there is excessive inflammatory
response which is poorly regulated

67. • Hypovolemic state, cardiac depression,
interstitial loss, AV shunt all causes cellular
hypoxia and ultimate septic shock

70. Clinical features
• Early stage- (compensated/warm shock) or
condition not associated with hypovolemia
- febrile(38-41)
- Shivering and malaise
- Warm dry flushed skin
- Hyperventilation
- Rapid bounding pulse
- Wide pulse pressure

71. Decompensated/cold shock
• Altered sensorium
• Cold clammy skin
• Feeble pulse
• Hypothermia
• Oliguria
• Jaundice
• UGI
• DIC

72. • Localizing infection
- A good systemic examination is done to detect
any focus of infection.

73. Diagnosis
• Blood/urine/sputum culture
• CBC
• BUN and Creatinine
• PT and PTT
• ECG
• Serum lactate dehydrogenase level
• Urinalysis
• ABG

74. Treatment
• Septic shock is a medical emergency that
requires prompt and sufficient resuscitation
• Treatment should be carried out in ICU setting
Aims
To improve hemodynamic state
Restore tissues perfusion
Eliminate toxin from body

75. 1) volume replacement
- Iv assess with large bore cannula
- Prompt investigation
- Crystalloids start: 1lit in 30 min-45min,
reassess and repeat appropriate
- Catherization
- CVP monitoring

76. • Vasopressor
2) Oxygen
3)Antibiotic
4) Steroid
5)NSAID
6)Free radical scavengers
7) Glycemic control
8) Naloxone
9) Coagulation
10) Surgery

77. WATCH
• Clinical sign
- Sensorium
- Conjunctiva
- Capillary refill
- Warm dry skin
• Urine output
• Vitals
• CVP
• Lungs and JVPABSG

78. Complication
• ARDS
• ARF
• DIC
• Encephalopathy
• Liver failure
• Coma
• Death

79. Prognosis
• Poor prognostic factor
- Advanced age
- Immunosuppression
- Infection
- Need for inotropes for >24hrs
- Availability and mode of treatment

80. Prevention
• Early recognition
• Prompt treatment of infection
• Meticulous surgical treatment
• Pre op antibiotics
• Aseptic technique

81. Treatment
• 1. Recognize signs of poor perfusion (0-5min)
• Decreased mental status
• Cold extremities
• Delayed capillary refill
• Weak pulses, differential central and peripheral
pulses
• Low urine output
• Hypotension or low BP: Minimum systolic BP by
age: < 1mo: 60 mmHg; 1mo to 10y: 70 + (2 × age
in years); ≥10y: 90 mmHg

82. 2. Assess ABCs (0-5 min)
• Provide 100% oxygen at high flow rate (15L)
• Early intubation may be necessary in neonates and infants
• Breathing assistance as necessary, including mechanical
ventilation
3. Establish IV access and place on monitor (0-5min)
• 2 large-bore peripheral IVs (PIVs) preferred: if difficult IV,
place IO access per PALS guidelines; 1 PIV may be sufficient
unless vasoactive drugs needed (see Step No. 6, below)
• Consider labs on IV placement: blood gas, lactate, glucose,
ionized calcium, CBC, cultures (glucose check through
finger stick preferred for rapid result)

83. 4. Fluid and electrolyte resuscitation (5-15min)
• Fluids:
• Push 20 mL/kg fluid (isotonic crystalloid) IV/IO over 5-
20min or faster if needed (reassess for signs of shock;
see Step No. 11, below)
• Repeat 20 mL/kg bolus push of fluid (up to 60 mL/kg)
until clinical symptoms improve or patient develops
respiratory distress/rales/ hepatomegaly
• May continue to require additional fluid above 60
mL/kg (fluid refractory) (see Step No. 6, below)
• Fluid needs may approach 200 mL/kg in warm septic
shock (warm extremities, flash capillary refill)

84. Correct hypoglycemia:
• Glucose levels in hypoglycemia: Neonates < 45 mg/dL;
infants/children < 60 mg/dL
• Glucose dosage: 0.5-1 g/kg IV/IO (max that can be
administered through a peripheral vein is 25% dextrose
in water) (see alternative treatments immediately
below)
• Treatment options to provide 0.5-1 g/kg glucose: For
infant/child: dextrose 25% in water: 2-4 mL/kg IV/IO;
dextrose 10% in water: 5-10 mL/kg IV/IO; for neonate:
dextrose 10% in water: 2-4 mL IV/IO; consider
maintenance fluid containing dextrose

85. Correct hypocalcemia for low ionized calcium:
• Calcium gluconate 100 mg/kg IV/IO (max 2g) PRN
• Calcium chloride 20 mg/kg IV/IO PRN ( Note: central
line administration preferred over 60min in nonarrest
situation)
5. Infection control (5-60min)
• Immediate considerations:
• Administer antibiotics immediately after cultures
obtained (blood, urine, +/- CSF/ sputum)
• Do not delay antibiotics because of delay in obtaining
cultures; initial antibiotics should be given within 1h

86. Neonates >2kg:
• Ampicillin plus gentamicin: Ampicillin for 0-7d:
50 mg/kg IV/IM/IO q8h; ampicillin >7d: 50 mg/kg
IV/IM/IO q6h plus gentamicin (dosing institution
dependent): 4mg/kg IV/IO/IM q24h (alternative
for 0-7d: 2.5 mg/kg IV/IO/IM q12h; alternative for
>7d: 2.5 mg/kg IV/IO/IM q8h) or
• Ampicillin plus cefotaxime: Ampicillin for 0-7d:
50 mg/kg IV/IM/IO q8h; ampicillin >7d: 50 mg/kg
IV/IM/IO q6h plus cefotaxime 50 mg/kg IV/IO q8h

87. Infants (>1mo) and children:
• Ceftriaxone 75 mg/kg (max 2g) IV/IO/IM
q24h plus vancomycin 15mg/kg (max 1g) IV/IO
q8h
Immunosuppressed patients:
• Vancomycin 15 mg/kg IV/IO (max 1 g/dose)
q8h plus cefepime 50 mg/kg IV/IO (max
2g/dose) q8h; consider antifungal therapy

88. 6. Fluid-refractory shock (persisting after 60 mL/kg fluid) (15-60 min)
• Continue fluid resuscitation and initiate vasopressor therapy titrated to
correct hypotension/poor perfusion
• Central line placement and arterial monitoring if not already established;
vasopressors should not be delayed for line placements
• Normotensive shock (impaired perfusion but normal blood pressure):
Dopamine 2-20 mcg/kg/min IV/IO, titrate to desired effect; if continued
poor perfusion, consider dobutamine infusion 2-20 mcg/kg/min IV/IO,
titrate to desired effect (may cause hypotension, tachycardia)
• Warm shock (warm extremities, flash capillary refill): Norepinephrine 0.1-
2 mcg/kg/min IV/IO infusion, titrate to desired effect
• Cold shock (cool extremities, delayed capillary refill): Epinephrine 0.1-1
mcg/kg/min IV/IO infusion, titrate to desired effect

89. 7. Shock persists following vasopressor initiation (60 min)
• Continued fluid replacement; obtain CVP measurement to guide
SvO2 < 70% (cold shock): Transfuse Hgb >10 g/dL; optimize arterial
saturation through oxygen therapy, ventilation; epinephrine 0.1-1
mcg/kg/min IV/IO infusion, titrate to desired effect
• SvO2 < 70% (normal BP but impaired perfusion): Transfuse Hgb >10
g/dL; optimize arterial saturation through oxygen therapy,
ventilation; consider addition of milrinone 0.25-0.75 mcg/kg/min
IV/IO (titrate to desired effect) ornitroprusside 0.3-5 mcg/kg/min
IV/IO (titrate to desired effect)
• SvO2 >70% (warm shock): Norepinephrine 0.1-2 mcg/kg/min IV/IO
infusion, titrate to desired effect; consider vasopressin 0.2-2
mU/kg/min infusion, titrate to desired effect

90. 8. Fluid refractory and vasopressor-dependent shock) (60
min)
• Consider adrenal insufficiency
• Hydrocortisone 2 mg/kg (max 100mg) IV/IO bolus; obtain
baseline cortisol level; if unsure, consider ACTH stimulation
test; duration depends on response, laboratory evaluation
9. Continued shock
• Consider cardiac output measurement to direct further
therapy
• Consider extracorporeal membrane oxygenation (ECMO)
10. Supplemental therapies

91. Neurogenic Shock

92. • Neurogenic shock is a medical condition which
occurs as a result of disturbance in the
sympathetic outflow causing loss of vagal tone
• Experiences neurogenic shock after injury to
the spinal cord and when there is disruption in
the blood circulation throughout the body due
to injury/ illness.
•

93. • It is a serious and life-threatening condition, which
requires prompt medical attention without any delay. If
the treatment is delayed, then it causes irreversible
tissue damage and even death.
• Out of the different types of the shocks, neurogenic
shock is the most difficult to manage, mainly because
of the irreversible damage to the tissues.
• Neurogenic shock mainly affects the spinal cord; the
function of which is transmitting neural signals from
the brain to the entire body and back.

96. • Most common causes is spinal injury above T
6.
• Most rare form of shock

97. sign
• Hypothermia, hypotension, decreased CO,
bradycardia, flaccid paralysis

98. Management
• Main aim is to prevent complication and
maintain perfusion

99. • Hypovolemic- with fluid
• Observe for fluid overload
• Vasopressors
• Hypothermia
• Treat hypoxia
• Maintain ventilator support

100. • Observe for bradycardia- major Dysarrthemia
• Observe for DVT- Venous pooling in
extremities make patients high risk
• Use prevention modalities

101. • Alpha agonist to augment tone if perfusion
still in adequate
• Dopamine(>10 mcg/kg per min)
• Ephedrie(12.5-25mg iv every 3-4 hour)
• Treat bradycardia with atropine 0.5-1mg doses
to maximum 3 mg
• May need transcutaneous or transv svenous
pacing temporarily