Pediatric Shock

Recognition, Classification and Initial Management

Critical Concepts Course

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

Hgb

CaO2

Influenced By

Oxygenation

A-a gradient DPG Acid-Base Balance Blockers Competitors Temperature

DO2
Influenced By

Drugs Conduction System

HR CO CVP Venous Volume Venous Tone

EDV SV Ventricular Compliance

Influenced By

ESV

Contractility

Metabolic Milieu Ions Acid Base Temperature Drugs Toxins Blockers Competitors Autonomic Tone

Influenced By

Afterload Temperature Drugs

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 is made through the physical examination focused on tissue perfusion
hypotension is a late and premorbid sign

Diagnosis

Abject

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 History

Past

medical history heart disease surgeries steroid use medical problems Brief history of present illness exposures onset

Differential Diagnosis of Shock

Cardiogenic
Myocardial dysfunction Dysrrhythmia Congenital heart

Hypovolemic
Hemorrhage Fluid loss Drugs

disease

Distributive
Analphylactic Neurogenic Septic

Obstructive
Pneumothorax,

CardiacTamponade, Aortic Dissection

Dissociative
Heat, Carbon

monoxide, Cyanide Endocrine

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.

Breathing
Always give 100% oxygen to start Sat monitor

Circulation
Establish IV access rapidly
CR 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 ringers (RL) Except for myocardial failure use 1020ml/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 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

Fluid in early septic shock

Carcillo, et al, JAMA, 1991

Group 1 Group 2 Group 3

(n = 14) Hypovolemic at 6 hours -Deaths Not hypovolemic at 6 hours -Deaths Total deaths 6 6 8 2 8 (n = 11) 2 2 9 5 7 (n = 9) 0 0 9 1 1

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

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

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

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.

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

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 liver Gallop rhythm Murmur Rales

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

Fluid Treat underlying cause

Management

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

CO SVR MAP Wedge CVP Or Hypovolemic Cardiogenic Or Or Obstructive Or Or Or Distributive Septic: Early Or or Septic: Late

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 Nelsons Textbook of Pediatrics Some slides based on works by Dr. Lou DeNicola and Dr. Linda Siegel for PedsCCM American Heart Association PALS guidelines