Shock states in children
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Pediatric Shock
Recognition, Classification and Initial Management
Ramin Nazari MDPediatric Critical Care FellowSt. Christopher Hospital for Children
December 2012
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Introduction
Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands
Oxygen delivery (DO2 ) is less than Oxygen Consumption (< VO2)
Untreated this leads to metabolic acidosis, organ dysfunction and death
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Oxygen Delivery
Oxygen delivery = Cardiac Output x Arterial Oxygen Content
(DO2 = CO x CaO2) Cardiac Output = Heart Rate x Stroke Volume
(CO = HR x SV) – SV determined by preload, afterload and contractility
Art Oxygen Content = Oxygen content of the
RBC + the oxygen dissolved in plasma (CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)
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Figure 1. FACTORS AFFECTING OXYGEN DELIVERY
DO2
CaO2
CO
SV
HR
Oxygenation
Hgb
A-a gradient DPG
Acid-Base Balance Blockers
Competitors Temperature
Drugs Conduction System
Ventricular Compliance
EDV
ESV Contractility
CVP Venous Volume
Venous Tone
Afterload Blockers Temperature Competitors Drugs Autonomic Tone
Metabolic Milieu Ions
Acid Base Temperature
Drugs Toxins
Influenced By
Influenced By
Influenced By
Influenced By
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Stages of Shock
Compensated– Vital organ function maintained, BP
remains normal. Uncompensated
– Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops.
Irreversible
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Clinical Presentation Early diagnosis requires a high index of
suspicion
Diagnosis is made through the physical examination focused on tissue perfusion
Abject hypotension is a late and premorbid sign
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Initial Evaluation: Physical Exam Findings of Shock
Neurological: Fluctuating mental status, sunken fontanel
Skin and extremities: Cool, pallor, mottling, cyanosis, poor cap refill, weak pulses, poor muscle tone.
Cardio-pulmonary: Hyperpnea, tachycardia.
Renal: Scant, concentrated urine
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Initial Evaluation: Directed History
Past medical history– heart disease– surgeries– steroid use– medical problems
Brief history of present illness
– exposures– onset
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Differential Diagnosis of Shock
HypovolemicHemorrhageFluid lossDrugs
DistributiveAnalphylacticNeurogenicSeptic
CardiogenicMyocardial dysfunctionDysrrhythmiaCongenital heart
disease Obstructive
Pneumothorax, CardiacTamponade, Aortic Dissection
DissociativeHeat, Carbon
monoxide, CyanideEndocrine
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Differential Diagnosis of Shock
Precise etiologic classification may be delayed
Immediate treatment is essential Absolute or relative hypovolemia is
usually present
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Neonate in Shock:Include in differential:
Congenital adrenal hyperplasia Inborn errors of metabolism Obstructive left sided cardiac lesions:
– Aortic stenosis
– Hypoplastic left heart syndrome
– Coarctation of the aorta
– Interrupted aortic arch
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Management-General Goal: increase oxygen delivery and
decrease oxygen demand:For all children:
○ Oxygen ○ Fluid ○ Temperature control○ Correct metabolic abnormalities
Depending on suspected cause:○ Antibiotics○ Inotropes○ Mechanical Ventilation
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Management-General
AirwayIf not protected or unable to be maintained,
intubate.
BreathingAlways give 100% oxygen to startSat monitor
CirculationEstablish IV access rapidlyCR monitor and frequent BP
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Management-General
Laboratory studies:– ABG– Blood sugar– Electrolytes– CBC– PT/PTT– Type and cross– Cultures
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Management-Volume Expansion Optimize preload Normal saline (NS) or lactated ringer’s
(RL) Except for myocardial failure use 10-
20ml/kg every 2-10 minutes. Reasses after every bolus.
At 60ml/kg consider: ongoing losses, adrenal insufficiency, intestinal ischemia, obstructive shock. Get CXR. May need inotropes.
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Fluid in early septic shockCarcillo, et al, JAMA, 1991
Retrospective review of 34 pediatric patients with culture + septic shock, from 1982-1989.
Hypovolemia determined by PCWP, u.o and hypotension.
Overall, patients received 33 cc/kg at 1 hour and 95 cc/kg at 6 hours.
Three groups:– 1: received up to 20 cc/kg in 1st 1 hour– 2: received 20-40 cc/kg in 1st hour– 3: received greater than 40 cc/kg in 1st hour
No difference in ARDS between the 3 groups
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Fluid in early septic shockCarcillo, et al, JAMA, 1991
Group Group 11(n = 14)(n = 14)
Group Group 22(n = 11)(n = 11)
Group Group 33(n = 9)(n = 9)
Hypovolemic Hypovolemic at 6 hours at 6 hours
-Deaths-Deaths
66
66
22
22
0 0
00
Not Not hypovolemic hypovolemic at 6 hours at 6 hours
-Deaths-Deaths
88
22
99
55
9 9
11
Total deathsTotal deaths 88 77 11
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FluidsSolution Na+ Cl- K+ Ca++ Mg++ BufferNS 154 154 0 0 0 NoneLR 130 109 4 3 0 Lactate Inotropic and vasoactive drugs are not a substitute for
fluid, however...Can have various combinations of hypovolemic and
septic and cardiogenic shockMay need to treat poor vascular tone and/or poor
cardiac function
18
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Inotropes and Vasopressors
Lack of history of fluid losses, history of heart disease, hepatomegaly, rales, cardiomegaly and failure to improve perfusion with adequate oxygenation, ventilation, heart rate, and volume expansion suggests a cardiogenic or distributive component.
Consider Appropriate inotropic or vasopressor support.
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Case 1
15-year-old previously well boy is freshly from the PICU, POD #3 from partial small bowel resection after multiple gunshot wounds to the abdomen. The nurse pages because his HR has increased in the last hour from 90 to 130, despite pain score of 1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP 80/50. Cap refill is >3 seconds in his cool extremities and pulses are 1+.
What is your assessment? What is the stage of shock? What is the classification of shock? What is your initial management?
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Hypovolemic Shock
Most common form of shock world-wide Results in decreased circulating blood
volume, decrease in preload, decreased stroke volume and resultant decrease in cardiac output.
Etiology: Hemorrhage, renal and/or GI fluid losses, capillary leak syndromes
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Hypovolemic Shock
Clinically, history of vomiting/diarrhea or trauma/blood loss
Signs of dehydration: dry mucous membranes, absent tears, decreased skin turgor
Hypotension, tachycardia without signs of congestive heart failure
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Hemorrhagic Shock
Most common cause of shock in the United States (due to trauma)
Patients present with an obvious history (but in child abuse history may be misleading)
Site of blood loss obvious or concealed (liver, spleen, intracranial, GI, long bone fracture)
Hypotension, tachycardia and pallor
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Hypovolemic/Hemorrhagic Shock:
Therapy
Always begin with ABCs Replace circulating blood volume
rapidly: start with crystalloid Blood products as soon as available for
hemorrhagic shock (Type and Cross with first blood draw)
Replace ongoing fluid/blood losses & treat the underlying cause
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SIRS/Sepsis/Septic shockSIRS/Sepsis/Septic shock
Mediator release:Mediator release:
exogenous & endogenousexogenous & endogenous
MaldistributionMaldistribution
of blood flowof blood flow
CardiacCardiac
dysfunctiondysfunction
Imbalance of Imbalance of oxygenoxygen
supply and supply and demanddemand
Alterations inAlterations in
metabolismmetabolism
Septic Shock
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Septic Shock: “Warm Shock” Early, compensated, hyperdynamic state Clinical signs
Warm extremities with bounding pulses, tachycardia, tachypnea, confusion.
Physiologic parameterswidened pulse pressure, increased cardiac
ouptut and mixed venous saturation, decreased systemic vascular resistance.
Biochemical evidence:Hypocarbia, elevated lactate, hyperglycemia
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Septic Shock: “Cold Shock”
Late, uncompensated stage with drop in cardiac output.
Clinical signsCyanosis, cold and clammy skin, rapid thready
pulses, shallow respirations. Physiologic parameters
Decreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leak
Biochemical abnormalitiesMetabolic acidosis, hypoxia, coagulopathy,
hypoglycemia.
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Cold Shock rapidly progresses to mutiorgan system failure or death if untreated
Multi-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DIC
More organ systems involved, worse the prognosis
Therapy: ABCs, fluid Appropriate antibiotics, treatment of underlying
cause
Septic Shock
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Case 2 6-year-old previously well girl is admitted to your ward directly
from clinic with fever, bloody diarrhea x 1 day. She’s had no urine x 24 hrs and is becoming harder to awaken. On exam, her HR is 150, BP 72/30, temp 103. She’s sleepy but
arousable. She’s flushed with capillary refill <1 second.
What is your assessment? What is the stage of shock? What is the classification of shock? What is your differential for the etiology? What is your initial management? If a higher level of care is needed,
how would you obtain it?
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Cardiogenic Shock
Etiology:– Dysrhythmias– Infection (myocarditis)– Metabolic– Obstructive– Drug intoxication– Congenital heart disease– Trauma
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Cardiogenic Shock
Differentiation from other types of shock:– History– Exam:
Enlarged liverGallop rhythmMurmurRales
– CXR: Enlarged heart, pulmonary venous congestion
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Cardiogenic Shock
Management:– Improve cardiac output::
Correct dysrhthymias Optimize preload Improve contractility Reduce afterload
– Minimize cardiac work: Maintain normal temperature Sedation Intubation and mechanical ventilation Correct anemia
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Case 3 4-month-old boy ex-term, previously well boy presents to ED
with decreased desire to feed x 2 days with 2 times daily emesis, following what sounds like viral URI. Urine output has been 3 wet diapers daily. He is afebrile with HR 180; BP has not been obtained. He has a weak cry, is mottled with 3-second capillary refill, pulses 1+ in all extremities. Liver is palpable 4 cm below RCM. S4 is present without murmur.
What is your assessment? What is the stage of shock? What is the classification of shock? What is your differential for the etiology? What is your initial management?
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Distributive Shock Due to an abnormality in vascular tone
leading to peripheral pooling of blood with a relative hypovolemia.
Etiology– Anaphylaxis– Drug toxicity– Neurologic injury– Early sepsis
Management– Fluid– Treat underlying cause
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Obstructive Shock
Mechanical obstruction to ventricular outflow
Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponade
Inadequate C.O. in the face of adequate preload and contractility
Treat underlying cause.
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Dissociative Shock
Inability of Hemoglobin molecule to give up the oxygen to tissues
Etiology: Carbon Monoxide poisoning, methemoglobinemia, dyshemoglobinemias
Tissue perfusion is adequate, but oxygen release to tissue is abnormal
Early recognition and treatment of the cause is main therapy
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Hemodynamic Variables in Different Shock States
or or Septic: Septic: LateLate
Or Or Septic: Septic: EarlyEarly
Or Or Or Or Or Or DistributivDistributivee
Or Or ObstructiveObstructive Or Or CardiogeniCardiogeni
cc
Or Or HypovolemiHypovolemicc
CVPCVPWedgWedgee
MAPMAPSVRSVRCOCO
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Final Thoughts Recognize compensated shock quickly- have a
high index of suspicion, remember tachycardia is an early sign. Hypotension is late and ominous.
Gain access quickly- if necessary use an intraoseous line.
Fluid, fluid, fluid - Administer adequate amounts of fluid rapidly. Remember ongoing losses.
Correct electrolytes and glucose problems quickly. If the patient is not responding the way you think
he should, broaden your differential, think about different types of shock.
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Take-Home Points
Shock is a progressive process. Intervene early.
Identifying the stage and classification of shock is important. Stage: Compensated, uncompensated, or irreversible? Classification: Hypovolemic, distributive, cardiogenic, or
obstructive?
Management should be directed at normalizing tissue perfusion and blood pressure. Consider using the consensus-based goal-directed algorithm for
shock management.
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