[PPT]Pediatric Shock - School of Medicine - LSU Health New...
Transcript of [PPT]Pediatric Shock - School of Medicine - LSU Health New...
Pediatric Shock
Critical Concepts Course
Recognition, Classification and Initial Management
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
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)
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
Stages of Shock
Compensated– Vital organ function maintained, BP
remains normal. Uncompensated
– Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops.
Irreversible
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
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
Initial Evaluation: Directed HistoryPast medical history
– heart disease– surgeries– steroid use– medical problems
Brief history of present illness
– exposures– onset
Differential Diagnosis of Shock Hypovolemic
HemorrhageFluid lossDrugs
DistributiveAnalphylacticNeurogenicSeptic
CardiogenicMyocardial dysfunctionDysrrhythmiaCongenital heart
disease Obstructive
Pneumothorax, CardiacTamponade, Aortic Dissection
DissociativeHeat, Carbon
monoxide, CyanideEndocrine
Differential Diagnosis of Shock
Precise etiologic classification may be delayed
Immediate treatment is essential Absolute or relative hypovolemia is
usually present
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
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
Management-General Airway
If not protected or unable to be maintained, intubate.
BreathingAlways give 100% oxygen to startSat monitor
CirculationEstablish IV access rapidlyCR monitor and frequent BP
Management-General Laboratory studies:
– ABG– Blood sugar– Electrolytes– CBC– PT/PTT– Type and cross– Cultures
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.
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
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
00Not Not hypovolemic hypovolemic at 6 hours at 6 hours -Deaths-Deaths
88
22
99
55
9 9
11
Total deathsTotal deaths 88 77 11
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.
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
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
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
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
SIRS/Sepsis/Septic shockSIRS/Sepsis/Septic shock
Mediator release:Mediator release:exogenous & endogenousexogenous & endogenous
MaldistributionMaldistributionof blood flowof blood flow
CardiacCardiacdysfunctiondysfunction
Imbalance of Imbalance of oxygenoxygen
supply and supply and demanddemand
Alterations inAlterations inmetabolismmetabolism
Septic Shock
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
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.
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
Cardiogenic Shock
Etiology:– Dysrhythmias– Infection (myocarditis)– Metabolic– Obstructive– Drug intoxication– Congenital heart disease– Trauma
Cardiogenic Shock Differentiation from other types of
shock:– History– Exam:
Enlarged liverGallop rhythmMurmurRales
– CXR: Enlarged heart, pulmonary venous congestion
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
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
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.
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
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
Recognition and Classification
Initial Management of Shock
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.
References, Recommended Reading, and Acknowledgments Uptodate: Initial Management of
Shock in Pediatric patients Nelson’s Textbook of Pediatrics Some slides based on works by Dr.
Lou DeNicola and Dr. Linda Siegel for PedsCCM
American Heart Association PALS guidelines