Shock in pediatric

EM1-K13

Shock

A state of circulatory dysfunction that fails to provide sufficient oxygen and nutritions to meet the metabolic needs of vital organs and peripheral tissues

Oxygen Delivery

DO2 = CaO2 x COCaO2 = (Hgb x 1.34 x SaO2) + (0.003 x PaO2)CO = HR x SV

Decreased DO2 - GlucoseDecreased ATP production

Loss of membrane integrity

K efflux, Na influx

Ca influx

Formation of damaging free radicals

Increases Nitric Oxide production

Activates proteases

Damages mitochondria

Damage cellular contents

Elaborated inflammatory mediators (eg, IL-1B, Tumor Necrosis Factor-α)

Microvascular thrombosis and loss of vascular integrity

Further edema formation

Cell death

Cellular edema

Pathophysiology of hypoxic-ischemic injury

Multiple system organ failure

Death

Disturbance cellular homeostasis

TachycardiaCool extremitiesProlonged capillary refillWeak peripheral pulsesNormal blood pressure

Depressed mental statusDecreased urine outputMetabolic acidosisTachypneaWeak central pulses

©Compensated

©Inadequate end organ perfusion

©Decompensated

Sign of shock state & progress

Hypotension

Major categories of shock

Hypovolemic

The most common type; circulating intravascular blood volume decrease; decrease in preload; decrease CO

Cardiogenic

Heart rate abnormalities (heart block, ventricular, supraventricular tachycardia), decreased myocardial contractility

Distributive

Relative uncommon; maldistribution of tissue blood flow due to decreased systemic vascular resistance,

ObstructiveExtrinsic force acting on intrathoracic structures (great vessels, ventricle)

Etiology and typical presentation of

Hypovolemic ShockEtiology Diarrhea

Blood loss (traumatic)

Presentation

Tachycardia Narrowed pulse

pressure Delayed capillary refill Cool extremities Late stages:

hypotension

Etiology and typical presentation of

Cardiogenic ShockEtiology CHD, cardiomyopathies, myocarditis, coronary infark

Dysrhytmia Acidosis, hypoxic-ischemic,

poisoning, metabolic disorders Prolonged shock Sepsis

Presentation

Bradycardia/tachycardia Gallop Barely perceptible pulses Cardiomegaly Rales

Etiology and typical presentation of

Distributive ShockEtiology Early septic Shock

Anaphylaxis Toxic ingestion Spinal/ epidural anesthesia Head/spinal cord injuries

Presentation Flush appearance Warm extremities Bounding pulses Tachycardia Wide pulse pressure Capillary refill may be

instantaneous

Etiology and typical presentation of

Obstructive ShockEtiology · CHD (Aortic stenosis/

coarctation)· Tension pneumothorax· Hemopneumothorax· Pericardial effusion

Presentation

· Tachycardia· Cool extremities· Delayed capillary refill· Narrow pulse pressure· Distended neck veins, distant

heart tones, asymmetric breath sounds

Evaluation of shock

· Assesment of Airway, breathing and circulation

· Blood glucose· History and physical examination

Assesment of airway, breathing and circulation

Airway · Airway patencyBreathing · Respiratory rate

· Respiratory pattern· Work of breathing (respiratory

distress)· Continuous pulse oxymetry

Circulation · Bradycardia· Tachycardia· Rhythm abnormalities· Central and distal pulse· Capillary refill (normal : complete

between 2 to 3 seconds)· Hypotension (late finding)

Normal respiratory rates in children

Age Respiratory rate (breaths/minute)

Newborn-1 year

30-60

1-3 years 25-403-12 years 20-30>12 years 12-20

Normal heart rates in children

Age Heart rate (beats/minute)

Newborn 80-200< 2 years 80-1802-10 years 60-150>10 years 60-100

Neonatal blood pressurebased on birth weight

Lower limit of systolic blood pressure by age

Age Systolic blood pressure (mm Hg)

Newborn 60< 1 years 701-10 years 70 + (age in years x 2) > 10 years 90

Blood glucose

· Bedside assessment· Infant are vulnerable to hypoglycemia· Hypoglycemia may result

severe/permanent neurologic disability

History and Physical Examination

· History· Serial assessment of vital signs, mentation,

and perfusion· Fever (serious infection?), hypothermia

(sepsis?)· The lung fields auscultation (rales :

hypervolemia?)· Gallop rhythm (underlying heart disease,

hypervolemia)· Palpation of liver edge below the costal

margin (hypervolemia, cardiac failure?)· Purpuric or petechial rashes (infectious?)· Secondary survey (injuries?)

1. ABC’s of life support2. Vascular access3. Fluid resuscitation 4. Inotropic-Vasoactive5. Control acidosis6. Monitoring, laboratory studies,

CXR7. Treat the underlying cause

Management of shock

ABC’s of life support

· Open airway· Suction· High Concentration O2· Assist ventilation (as needed)· Control bleeding· Shock position· Keep warm

· Use isotonic crystalloid solution (eg, lactated Ringer’s solution or normal saline) or 5 % albumine.

· Fluid boluses, 20 mL per kg, severe : 40-60 ml/kg, max 200 ml/kg rapidly until the shock is resolved (delivered in 5-10 minutes)

· Observing for signs of fluid overload (increased work of breathing, rales, gallop rhythm, or hepatomegaly)

· Use a glucose-containing solution to only treat documented hypoglycemia

· Correct hypocalcemia· Insufficient data to recommendation or

against using hypertonic saline for shock associated with head injuries or hypovolemia

Fluid resuscitation

Inotropes-Vasoactive agents is use if shock requiring pharmacologic improvement of cardiac contractility function or decompensated shock refractory to volume expansion alone

Inotropes-Vasoactive

Inotropes/Vasoactive AgentsDopamine 1-5 mcg/kg/min: dopaminergic; 5-15

mcg/kg/ min: more beta-1; 10-20 mcg/kg/min: more alpha-1

Dobutamine 2.5-15 mcg/kg/min; mostly beta-1, some beta-2

Epinephrine 0.05-0.1 mcg/kg/ min: mostly beta-1, some beta-2; >0.1 to 0.2 mcg/ kg/min: alpha-1

Nor-epinephrine 0.05-0.2mcg/kg/ min; Use up to 1mcg/kg/min; only alpha and beta-1

Milrinone 50mcg/kg load then 0.375-0.75 mcg/kg/min; Phosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effect on pulmonary vasculature)

Control acidosis

· Metabolic acidosis may become evident as child’s condition worsen

· Na Bic no longer routinely recommended because the use of Na Bic may increase intracellular acidosis

· Fluid resuscitation, vasoactive infusion and adequate ventilation/oxygenation are the main management

· Tromethamine /THAM given slowly (3-5 ml/kg) may use in extreme condition (i.e. pH < 7)

Monitoring, lab studies, and CXR

· Monitoring HR, BP continuously· Clinical evaluations/5 min until the patient is

stable· Urine output monitoring with an indwelling

catheter· Lab : ABG, serum electrolytes, glucose, Ca

levels, CBC, PT/PTT, blood type/cross match, and culture

· Evaluate ET tube position, heart size, and pulmonary status by CXR

Treat the underlying cause

· Trauma: ongoing bleeding may need to be addressed surgically

· Myocardial failure: inotropic medications· Sepsis: isolated and treat the infectious

organism with appropriate AB’s