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Pediatric Shock

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Title: Pediatric Shock Author: NCC Last modified by: Jennifer L. Avegno Created Date: 3/1/1999 6:23:08 PM Document presentation format: On-screen Show (4:3) – PowerPoint PPT presentation

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Title: Pediatric Shock


1
Pediatric Shock
Recognition, Classification and Initial
Management
Critical Concepts Course
2
Introduction
  • Shock is a syndrome that results from inadequate
    oxygen delivery to meet metabolic demands
  • Oxygen delivery (DO2 ) is less than Oxygen
    Consumption (lt VO2)
  • Untreated this leads to metabolic acidosis, organ
    dysfunction and death

3
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)

4
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5
Stages of Shock
  • Compensated
  • Vital organ function maintained, BP remains
    normal.
  • Uncompensated
  • Microvascular perfusion becomes marginal. Organ
    and cellular function deteriorate. Hypotension
    develops.
  • Irreversible

6
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

7
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

8
Initial Evaluation Directed History
  • Past medical history
  • heart disease
  • surgeries
  • steroid use
  • medical problems
  • Brief history of present illness
  • exposures
  • onset

9
Differential Diagnosis of Shock
  • Cardiogenic
  • Myocardial dysfunction
  • Dysrrhythmia
  • Congenital heart disease
  • Obstructive
  • Pneumothorax, CardiacTamponade, Aortic Dissection
  • Dissociative
  • Heat, Carbon monoxide, Cyanide
  • Endocrine
  • Hypovolemic
  • Hemorrhage
  • Fluid loss
  • Drugs
  • Distributive
  • Analphylactic
  • Neurogenic
  • Septic

10
Differential Diagnosis of Shock
  • Precise etiologic classification may be delayed
  • Immediate treatment is essential
  • Absolute or relative hypovolemia is usually
    present

11
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

12
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

13
Management-General
  • Airway
  • If not protected or unable to be maintained,
    intubate.
  • Breathing
  • Always give 100 oxygen to start
  • Sat monitor
  • Circulation
  • Establish IV access rapidly
  • CR monitor and frequent BP

14
Management-General
  • Laboratory studies
  • ABG
  • Blood sugar
  • Electrolytes
  • CBC
  • PT/PTT
  • Type and cross
  • Cultures

15
Management-Volume Expansion
  • Optimize preload
  • Normal saline (NS) or lactated ringers (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.

16
Fluid in early septic shock Carcillo, 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

17
Fluid in early septic shock Carcillo, et al,
JAMA, 1991
Group 1 (n 14) Group 2 (n 11) Group 3 (n 9)
Hypovolemic at 6 hours -Deaths 6 6 2 2 0 0
Not hypovolemic at 6 hours -Deaths 8 2 9 5 9 1
Total deaths 8 7 1
18
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.

19
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

20
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

21
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

22
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

23
Septic Shock
SIRS/Sepsis/Septic shock
Mediator release exogenous endogenous
Maldistribution of blood flow
Cardiac dysfunction
Imbalance of oxygen supply and demand
Alterations in metabolism
24
Septic Shock Warm Shock
  • Early, compensated, hyperdynamic state
  • Clinical signs
  • Warm extremities with bounding pulses,
    tachycardia, tachypnea, confusion.
  • Physiologic parameters
  • widened pulse pressure, increased cardiac ouptut
    and mixed venous saturation, decreased systemic
    vascular resistance.
  • Biochemical evidence
  • Hypocarbia, elevated lactate, hyperglycemia

25
Septic Shock Cold Shock
  • Late, uncompensated stage with drop in cardiac
    output.
  • Clinical signs
  • Cyanosis, 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 abnormalities
  • Metabolic acidosis, hypoxia, coagulopathy,
    hypoglycemia.

26
Septic Shock
  • 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

27
Cardiogenic Shock
  • Etiology
  • Dysrhythmias
  • Infection (myocarditis)
  • Metabolic
  • Obstructive
  • Drug intoxication
  • Congenital heart disease
  • Trauma

28
Cardiogenic Shock
  • Differentiation from other types of shock
  • History
  • Exam
  • Enlarged liver
  • Gallop rhythm
  • Murmur
  • Rales
  • CXR
  • Enlarged heart, pulmonary venous congestion

29
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

30
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

31
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.

32
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

33
Hemodynamic Variables in Different Shock States
34
Recognition and Classification
35
Initial Management of Shock
36
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.

37
References, Recommended Reading, and
Acknowledgments
  • Uptodate Initial Management of Shock in
    Pediatric patients
  • Nelsons Textbook of Pediatrics
  • Some slides based on works by Dr. Lou DeNicola
    and Dr. Linda Siegel for PedsCCM
  • American Heart Association PALS guidelines
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