2. 2
Out lines
ï± Definition
ï± Review of basic physiologic aspects
ï± Epidemiology of shock
ï± Pathophysiology
ï± Classification by type & severity
ï± Approach & Management
ï± References
3. SHOCK: Definition
âą Shock is an acute process characterized by
the bodyâs inability to deliver adequate
oxygen to meet the metabolic demands of
vital organs and tissues.
â Significant reduction of systemic tissue perfusion,
resulting in decreased tissue oxygen delivery
3
6. Oxygen Delivery
âą Oxygen Delivery
=> Cardiac Output x Arterial Oxygen
Content
âą Arterial Oxygen Content
=> Oxygen content of the RBC + the oxygen
dissolved in plasma
6
7. Epidemiology
âą Shock occurs in approx. 2% of all hospitalized
infants, children, & adults in developed countries
âą The mortality rate varies based on the
etiology and clinical circumstances.
âą Mortality from shock is less among children than
adults. For children with severe sepsis, mortality is
about 10 %, in comparison to 35 to 40 % within
one month of the onset of septic shock for adults.
7
8. Epidem....
âą Nevertheless, outcomes for children with
shock (in terms of morbidity & cost) are
significant.
âą Hypovolemic shock, the most
common cause of shock in children
world wide
â Which is most frequently caused by
Diarrhoea, Vomiting, or Haemorrhage
8
9. Pathophysiology of Shock
9
The combination of a continued presence of an inciting trigger and
the bodyâs exaggerated and potentially harmful neurohumoral,
inflammatory, and cellular responses leads to the progression of
shock.
10. Types of Shock (Etiologically)
1. Hypovolemic shock
2. Distributive shock
a. Septic Shock
b. Anaphylactic Shock
c. Neurogenic Shock
3. Cardiogenic shock
4. Obstructive shock
10
11. Types of Shock
Type of
Shock
Pathophysiology Signs & Symptoms
Hypovolem
ic
âPRELOAD: âCO,
âSVR,
intravascular
volume loss
âHR, â pulses, delayed RF,
dry skin, sunken eyes, oliguria
Distributive â AFTERLOAD
(SVR)
Anaphylacti
c
â CO, âSVR
Angioedema, low BP,
wheezing, respiratory distress
Spinal Normal CO, âSVR Low BP without tachycardia;
paralysis,
Septic Variable More to come
Cardiogenic âCO, Variable SVR Normal to âHR, âpulses, 11
13. Cardiogenic Shock
ï±Cardiac output falls due to the pathology in the
heart itself & is defined as CI < 2.2 L/min/m2.
âą Cardiac Pump Failure 20
to poor myocardial function
âą Manifested physiologically as systolic function & CO.
âą Cardiogenic shock is uncommon among children than
adults
âą Diverse mechanisms can be divided into 3 general categories:
1. Cardiomyopathies
2. Arrhythmias : Structural Heart Disease,
Drug Intoxications, and Hypothermia are
leading causes of arrhythmia in children
3. Obstructive disorders
13
14. Distributive Shock: causes
âą Is a state of abnormal vasodilatation & decreased SVR.
ïŒ Abnormal Vessel Tone (decreased after load)
ïŒ Sepsis: gram-negative sepsis, other infections
ïŒ Anaphylaxis
ïŒ Neurogenesis (Spinal)
ï± Spinal cord transection
ï± Anesthesia
ï± Drug overdose
ïŒ Drug intoxication (Diuretics), hypoxia, poisoning
14
18. Hemorrhagic Shock classification by
Severity
âą Four classes based upon % loss of blood volume.
âą As with nonhemorrhagic losses, clinical features
are typically used to estimate BV deficit.
âą Many children with class II hemorrhage, and
âą All of those with classes III & IV are in shock.
18
19. Hemorrhage Severity Classification
19
Classe
s
% of fluid
Loss
Symptomss/Signs Treatment
I Up to 15% Minimal physiologic changes are evident Crstalloid fluid
II 15-30% Mild tachycardia & tachypnea with a
narrow PP, slightly DCR, decreased
UOP, & mild anxiety.
Crstalloid fluid
May require Blood
products
III 30-40% Tachycardia, Tachypnea,
Hypotension, DCR, Altered
Mentation, Oliguria
Crstalloid solution &
Most Pt Need Blood
IV >40% Usually cold & pale with profoundly
depressed mentation, marked tachypnea
& tachycardia, and anuria.
Quick Blood products
Operative Intervention
often necessary to
control haemorrhage
20. Hypovolemic Shock
ï¶Clinical symptoms
âą Often manifests initially as orthostatic
hypotension and is associated with
ï± Dry mucous membrane, dry axillae
ï± Sunken fontanel/eyes
ï± Poor skin turgor
ï± DCR, Cool extremities
ï± Low or no urine output
âą Tachycardia => compensated shock!
âą Normal BP until volume loss >30-40%
âą Further volume loss and exacerbation of shock by
pre-existing low plasma oncotic pressure 20
21. ⹠Hypotension is typically a late finding among
children in shock.
âą For children, hypotension is defined as a
systolic blood pressure < 5th
percentile of
normal for age:
â < 60 mmHg in term neonates
â < 70 mmHg in infants
â < 70 mmHg + 2x age in years in 1 to 10
years
â < 90 mmHg in children >10 years of age
21
22. C/M ... General
âą Regardless of etiology, in uncompensated shock,
late in the progression of disease:
â Hypotension
â High SVR
â Decreased cardiac output
â Respiratory failure
â Obtundation, and
â Oliguria
â Elevated blood lactate levels
âą Reflect poor tissue oxygen delivery in all forms of
shock. 22
23. âą Additional clinical findings in shock include:
â Cutaneous lesions such as
âą Petechiae
âą Diffuse erythema
âą Ecchymoses
âą Ecthyma gangrenosum and
âą Peripheral gangrene
23
30. 3. Irreversible (Refractory) shock
âą It occurs as a consequence of decompensated
shock not managed properly and at right time.
âą Permanent cellular damage & MODS.
âą Recovery does not occur even with adequate
restoration of circulatory volume
âą Death occurs due to:
â Refractory Acidosis, Myocardial & Brain
Ischemia.
30
31. Complications of Shock
The main complications of severe shock
are:
1. Shock Lung (ARDS)
2. Acute Renal Failure
3. Gastrointestinal Ulceration
4. Disseminated Intravascular Coagulation
5. Multisystem Organ Failure
6. Death
31
33. Goals of the initial Evaluation of
Shock
ï±Immediate identification of life-threatening
conditions.
(eg, tension pneumothorax, hemothorax, cardiac
tamponade, or pulmonary embolism).
ï±Rapid recognition of circulatory compromise.
ï±Early classification of the type and cause of shock.
35. AppearanceÂ
ï¶Â Significant changes in appearance
like:
ïŒpoor tone
ïŒunfocused gaze indicators of decreased cerebral
perfusion.
ïŒweak cry
ï¶Subtle differences in appearance
decreased responsiveness to caretakers & painful
procedures.
36. BreathingÂ
ïŒA child with depressed mental status as the result
of shock may not be able to maintain a patent
airway.
ïŒ Tachypnea without respiratory distress can
develop in response to metabolic acidosis.
ïŒChildren with cardiogenic shock typically have
some increased work of breathing in addition to
tachypnea.
37. Circulation
ï Quality of central and peripheral pulsesÂ
ï§ Decreased intensity of distal pulses in comparison to
central pulses suggests peripheral vasoconstriction and
compensated shock.
ï§ Bounding pulses may be present in patients with
distributive (âwarmâ) shock.
ï Skin temperatureÂ
ï§ Skin may be mottled or cool in children with
compensated shock.
ï§ This finding can also be influenced by environmental
temperature.
38. ConâŠ
ï Capillary refillÂ
ï§ >2seconds .
ï§ Flash capillary refill (<1 second)
ï§ The usefulness of capillary refill is limited by:
âą inter-observer variability.
âą environmental temperature.
ïHeart rateÂ
ï§ Tachycardia ( compensated shock )
ï§ Bradycardia (Hypoxia, spinal cord injury and some
drugs).
39. History
1. Hx of injurey
2. A history of fluid loss
3. Fever and/or immunocompromised
4. A history of exposure to an allergen
5. Hx of exposure to toxins
6. Patients with chronic heart disease
7. risk for adrenal insufficiency
40. Approach to the classification of undifferentiated
shock in children, Does a child has�
41.
42. Physical Examination
V/S
âąAbnormal V/S provide essential information regarding :
â Severity, classification & cause of shock.
A.RRÂ âusually tachypneic.
B.HRÂ
o sinus tachycardia (except cardiogenic shock from a
brady arrhythmia or spinal cord injury).
o In compensated shock, it may be the only abnormal
vital sign.
o Other causes of tachycardia with poor perfusion in
children include: (SVT & VT)
43. ConâŠ
C. BP : normal / low BP.
D. T° : Fever (hypothermia in young infants)
E. Others: Stridor, wheezing (anaphylaxis).
C.Crackles (pneumonia, septic shock / HF, cardiogenic
shock).
D.Distended neck veins (HF, or cardiac tamponade or
tension pneumonia- or hemothorax).
E.Abnormal heart sounds (Â murmurs or a gallop rhythm
/ muffled heart tones
F.Pulse differentialÂ
G.HepatomegalyÂ
51. Shock Management Principles
1. Supportive Care
â ABC of Life
â Intubation, mechanical ventilation, Oxygen as
needed
1. Fluid Management
2. Treatment of underlying causes
51
52. Initial Management
âą Early recognition and prompt intervention are
extremely important in the management of all
forms of shock.
âą Regardless of the cause: ABC Donât Ever Forget
Glucose
âą Baseline mortality is much lower in pediatric
shock than in adult shock i.e due to early
interventions.
53. key steps to manage shock
1. Give oxygen (for infants 0.5 -1 l/min, older children 1-
2 l/min).
2. Give 10% Glucose 5 ml/kg by IV.
3.Keep the child warm.
4.Direct manual pressure to control
bleeding.
5. Take blood samples for emergency laboratory tests
6. Give IV fluids
7. First assess the child for severe malnutrition before
selecting treatment.
54. Intravenous Fluids
A. Shock With NO SAM
ï¶Fluid bolus of 20ml/kg isotonic fluid (maximum of 3X)
ï¶ If there is still NO improvement:
ïŒConsider Blood Transfusion unless there is profuse
watery diarrhea.
ïŒIn this case, repeat Ringer's lactate.
ï¶ If shock remains refractory following 60-80 mL/kg of
volume resuscitation, vasopressor therapy (norepinephrine,
or epinephrine) .
55. B. Child With SAM
âą The severely malnourished child is considered to have
shock if he/she is lethargic or unconscious and has
cold hands plus either:
â slow capillary refill (>3seconds), or
â weak, fast or absent radial or femoral pulses and
â absence of signs of heart failure in an edematous child.
56. ConâŠ
ï Weight a child.
ï IV Fluid (15ml/kg over 1hr).
ï Give normal saline or Ringer lactate with 5% glucose.
ï check PR and RR every 5-10 minutes.
ï If improved, change the IV fluid with oral intake/
Resomal after 2 hr.
ï If there is improvement: Repeat 15ml/kg over 1 hr.
57. ConâŠ
ïIf there is NO improvement:
ï§ Call senior health worker.
ï§ Give maintenance IV fluid 4ml/kg/hr while
waiting for blood.
ï§ Transfuse fresh whole blood at 10ml/kg slowly
over 3 hrs.
ï§ use packed cells, if in cardiac failure.
58. ConâŠ
ï Monitor with the Multi-chart and shock follow up chart.
ï Use one of the following solutions, listed in order of
preference:
ï§ Ringerâs lactate solution with 5% glucose*
ï§ 0.9 per cent normal saline with 5% glucose*
(add 125 ml of 40 % or 100 ml of 50% glucose to 1
liter of 0.9% saline to make this fluid)
ï *If either of these are used, add sterile potassium chloride
(20 Mmol/l) if possible.
ï Observe the child and check RR and PR every 10 minutes.
59. ConâŠ
âą If the RR (by 5 BPM) and PR (by 25 PPM) increase and child is
gaining weight.
â stop the IV rehydration & assume septic or cardiogenic
shock.
âą If RR & PR are slower after 1hour, the child is improving.
â Repeat the same amount of IV fluids for another hour.
â Continue to check RR & PR every 10 minutes.
âą After two hours of IV fluids, switch to oral or NG rehydration with
ReSoMal.
âą Give 5-10 ml/kg ReSoMal in alternate hrs. with F-75 for up to 10
hrs or until fully rehydrated.
60. A- HYPOVOLEMIC SHOCK
TREATMENT
GOAL â restore circulating volume and tissue
perfusion & correct the cause
1. Assess airway.
2. Administer oxygen.
3. Give IV Fluid bolus of 20ml/kg isotonic fluid
(maximum of 3) .
In case of shock refractory to fluids, start inotrope
(dopamine).
61. B- septic shock
Provide broad-spectrum antimicrobial agents.
ï Neonates (ampicillin plus cefotaxime and/or
gentamicin).
ïintraabdominal process is suspected, anaerobic
coverage ,such as metronidazole, clindamycin, or
piperacillin-tazobactam.
ïNosocomial sepsis ( 3rd- or 4th-generation
cephalosporin or a penicillin with an extended
Gramnegative spectrum). e.g., piperacillin-tazobactam.
62. ConâŠ
ï±community-acquired infections with Neisseria
meningitidis (3rd-generation cephalosporin,
(ceftriaxone or cefotaxime)).
ï±resistant Streptococcus pneumoniae & MRSA require
the addition of vancomycin.
ï±immunocompromised patients (Empirical coverage for
fungal infections).
63. C- Distributive shock
ïŒprimary abnormality in vascular tone.
ïŒmay benefit temporarily from volume
resuscitation.
ïŒearly initiation of a vasoconstrictive agent to
increase SVR .
64. conâŠ
1. ANAPHYLACTIC SHOCK
ïŒAirway, Withdrawal of Ag, Cautious fluid
administration
ïŒIV epinephrine
ïŒAntihistamine
ïŒCorticosteroids
ïŒVasopressors or Inotropes
65. ConâŠ
2. NEUROGENIC SHOCK
ïŒCautious fluid administration
ïŒVasopressors & Inotropes
ïŒCorrect hypothermia
ïŒTreat bradycardia with atropine
ïŒObserve and prevent DVT.
âąMay benefit from :phenylephrine or vasopressin
to increase SVR.
66. D- cardiogenic shock RX
GOAL :
increase CO, treat reversible causes& decrease myocardial
workload
1. Assess airway , administer oxygen /mechanical ventilation
2. Inotropic agents, vasoactive drugs.
3. IV fluids (5-10ml/kg boluses over longer time)
4. Morphine to decrease preload and anxiety
5. Short acting beta blockers for refractory tachycardia
67. E- obstructive shock
âą fluid resuscitation may be briefly temporizing in
maintaining cardiac output.
âą primary insult must be immediately addressed.
Such asâŠ
â pericardiocentesis for pericardial effusion,
â pleurocentesis for pneumothorax
â thrombectomy/thrombolysis for PE.
â prostaglandin infusion for ductus-dependent
cardiac lesions.
68.
69. Dopamine
ï± Low-dose: 1 to 5 mcg/kg/minute, results in increased renal blood
flow and urine output
ï± Intermediate-dose: 5 to 10 mcg/kg/minute, results in increased
renal blood flow, heart rate, cardiac contractility, and cardiac output
ï± High-dose: >10 mcg/kg/minute, alpha-adrenergic effects begin to
predominate, resulting in vasoconstriction, increased blood pressure
in addition to increased heart rate, cardiac contractility, and cardiac
output due to beta-adrenergic effects.
70.
71. Physiologic indicators and target goals
After the initial fluid bolus, evaluate for:
1) Quality of central and peripheral pulses (strong,
distal pulses equal to central pulses)
2) Skin perfusion (warm, with capillary refill <2
seconds)
3) Mental status (normal mental status)
4) Urine output (â„1 mL/kg per hr)
5) BP (systolic pressure at least fifth percentile for
age)
72. PROGNOSIS
ï± In septic shock, mortality rates are as low as 3% in
previously healthy children and 6-9% in children with
chronic illness (compared with 25-30% in adults).
ï± This is due to early recognition and therapy.
ï± But still shock and MODS remain one of the leading
causes of death in infants and children.
ï± The risk of death depends on:
ï§ underlying etiology.
ï§ presence of chronic illness.
ï§ host immune response.
ï§ timing of recognition and therapy.
73. References
1. NELSON TEXTBOOK OF PEDIATRICS 20TH
&
21th EDITION.
2. UPTODATE 2018.
3. PEDIATRIC HOSPITAL CARE: ETHIOPIA
(SECOND EDITION, 2016).
4. GUIDELINES FOR THE MANAGEMENT OF
ACUTE MALNUTRITION, FMOH, 2016.
73Shock Seminar: By Firomsa D &
G/Tsadik E
Shock is the physiologic state characterized by significant reduction of systemic tissue perfusion, resulting in decreased tissue oxygen delivery.
Furthermore, unique physiologic responses to poor perfusion among children make it a challenge for clinicians to recognize shock early (before hypotension develops), when responses to treatment are more favourable.
Most patients who do not survive, do not die in the acute hypotensive phase of shock, but rather as a result of associated complications and multiple
organ dysfunction syndrome (MODS).
MODS
Defined as any alteration of organ function that requires medical support for maintenance, and
the presence of MODS in patients with shock substantially increases the probability of death.
While decreased perfusion directly reflects decreased cardiac output, the increased cardiac output observed in hyperdynamic shock states also is associated with decreased effective tissue perfusion.
This decreased effective perfusion derives from a complex interaction of numerous humoral and microcirculatory processes resulting in patchy, uneven local regional blood flow and a derangement of cellular metabolic processes
Cardiogenic shock
Cardiac output falls due to the pathology in the heart itself & is defined as cardiac index &lt; 2.2 L/ minute/m2.
(Cardiac index is cardiac out put per meter of body surface area)
Cardiac Pump Failure 20 to poor myocardial function
Manifested physiologically as decreased systolic function & depressed CO.
Cardiogenic shock is uncommon among children, as compared with adults
The mechanisms are diverse can be divided into three general categories:
Cardiomyopathies
Arrhythmias
 Structural Heart Disease, Drug Intoxications, and Hypothermia are leading causes of arrhythmia in children
Obstructive disorders
Myocarditis
Cardiomyopathy,
Congenital Heart Disease, Or
Following Cardiac Surgery.
In these instances, myocardial contractility is affected, leading to Systolic and/or Diastolic dysfunction.
The later phases of all forms of shock frequently have a negative impact on the myocardium, leading to development of a cardiogenic component
to the shock state.
Distributive Shock
This process leads to significant decreases in both preload and afterload.
Therapies for distributive shock must address both of these problems simultaneously.
Anaphylaxis
An immediate, potentially life-threatening systemic reaction to an exogenous stimulus, typically an allergic, IgE-mediated immediate hypersensitivity reaction.
Anaphylactoid responses are clinically indistinguishable reactions that occur by nonantigen/antibody-mediated mechanisms.Â
Neurogenic shock
A rare, usually transient disorder that follows acute injury to the SC or CNS, resulting in loss of sympathetic venous tone.
The underlying pathophysiologic mechanism leading to distributive shock is a state of abnormal vasodilation and decreased SVR.
Septic shock is often a unique combination of distributive, Hypovolemic, and cardiogenic shock.
Hypovolemia from intravascular fluid losses occurs through capillary leak.
Cardiogenic shock results from the myocardial-depressant effects of sepsis
Distributive shock is the result of decreased SVR.
The degree to which a patient exhibits each of these responses varies, but there are frequently alterations in preload, afterload, and myocardial contractility.
Septic Shock
Severe sepsis plus the persistence of hypoperfusion or hypotension despite adequate fluid resuscitation or a requirement for vasoactive agents
(Sepsis plus cardiovascular organ dysfunction)
Sepsis is defined as SIRS resulting from a suspected or proven infectious etiology.
In the early stages (hyperdynamic phase, low SVR, or âWarmâ Shock), cardiac output increases in an attempt to maintain adequate oxygen delivery and meet the greater metabolic demands of the organs and tissues.
As septic shock progresses, cardiac output falls in response to the effects of numerous inflammatory mediators, leading to a compensatory elevation in SVR and the development of âColdâ Shock.
Coarctation of the aorta or
Hypoplastic LV Syndrome
Class IÂ âacute loss of up to 15 % of the child&apos;s BV. Minimal physiologic changes are evident and patients usually respond well to crystalloid fluid.
Class IIÂ â15 to 30 % blood loss. Physiologic changes include mild tachycardia and tachypnea with a narrow PP, slightly delayed capillary refill, decreased UOP, and mild anxiety.
Patients can usually be stabilized with crystalloid, or may require blood products.
Class IIIÂ â Class III hemorrhage is the result of an acute blood loss of 30 to 40 percent. Signs of shock (including tachycardia, tachypnea, hypotension, delayed capillary refill, altered mental status, and oliguria) are present. Prompt resuscitation with crystalloid solution & most patients will need blood products as well.
Class IVÂ âoccurs with &gt;40 % acute blood loss. Signs of shock are obvious and immediately life-threatening. Patients are usually cold and pale with profoundly depressed mentation, marked tachypnea and tachycardia, and anuria. Children should quickly receive blood products. Operative intervention is often necessary to control hemorrhage.
When there is preexisting low plasma oncotic pressure
(caused by NS, Malnutrition, Hepatic Dysfunction, Acute Severe Burns, etc.), even further volume loss and exacerbation of
shock may occur because of endothelial breakdown and worsening capillary leak.
Jaundice can be present either as a sign of infection or as a result of MODS.
Initial : The cells become leaky and switch to anaerobic metabolism.
Non-progressive:(Compensated Stage)
Attempt to correct the metabolic upset of shock.
Progressive: (Decompensated Stage )
Eventually the compensation will begin to fail.
Refractory :
Organs fail and the shock can no longer be reversed.
Multiorgan Failure:
Is any alteration of organ function that requires medical support for maintenance, and the presence of MODS in patients with shock substantially increases the probability of death.
Criteria for Organ Dysfunction
Cardiovascular
Despite administration of isotonic intravenous fluid bolus â„60 mL/kg in 1 hr: decrease in BP (hypotension) systolic BP &lt;90 mm Hg, mean arterial pressure &lt;70 mm Hg, &lt;5th percentile for age, or systolic BP &lt;2 SD below normal for age
or
Need for vasoactive drug to maintain BP in normal range (dopamine &gt;5 ÎŒg/kg/min or dobutamine, epinephrine, or norepinephrine at any dose)
or
Two of the following:
Unexplained metabolic acidosis: base deficit &gt;5.0 mEq/L
Increased arterial lactate: &gt;1 mmol/Liter or &gt;2Ă upper limit of normal
Oliguria: urine output &lt;0.5 mL/kg/hr
Prolonged capillary refill: &gt;5 sec
Core to peripheral temperature gap &gt;3°C (5.4°F)
Respiratory
PaO2/FIO2 ratio &lt;300 in absence of cyanotic heart disease or pre-existing lung disease
or
PaCO2 &gt;65 torr or 20 mm Hg over baseline PaCO2
or
Need for &gt;50% FIO2 to maintain saturation â„92%
or
Need for nonelective invasive or noninvasive mechanical ventilation
Neurologic
GCS score â€11
or
Acute change in mental status with a decrease in GCS score â„3 points from abnormal baseline
Hematologic
Platelet count &lt;100,000/mm3 or a decline of 50% in the platelet count from the highest value
recorded over the last 3 days (for patients with chronic hematologic or oncologic disorders)
or
INR &gt;1.5
or
Activated PT &gt;60 sec
Renal
Serum creatinine &gt;0.5 mg/dL,
â„2Ă upper limit of normal for age,
or
2-fold increase in baseline creatinine value
Hepatic
Total bilirubin â„4 mg/dL (not applicable for newborn)
Alanine transaminase level 2Ă upper limit of normal for age
ARDS as defined by the presence of a PaO2/FIO2 ratio â€300 mm Hg, bilateral infiltrates on chest radiograph, and no evidence of left heart failure
or
Sepsis plus 2 or more organ dysfunctions (respiratory, renal, neurologic, hematologic, or hepatic)