Critical Care Medicine

Pediatric Shock - Assessment and Treatment

Pediatric Shock - Assessment and Treatment

Shock is an acute disruption of circulatory function leading to the inadequate delivery of nutrients to tissues (SUPPLY<<<DEMAND).

  • A low blood pressure is not diagnostic, especially in children: given remarkable ability to compensate.

Related Conditions

Immunocompromised

Systemic Inflammatory Response Syndrome

Secondary adrenal insufficiency

1. Description of the problem

What every clinician needs to know

  • Oxygen delivery = cardiac output x oxygen content

  • Best way to increase oxygen content is to transfuse PRBCS not increase FiO2, unless severely anemic

  • Remember shock is not a blood pressure diagnosis

    • Clinical exam consistent with poor perfusion are KEY

  • A steadily rising HR is a key change in vital signs

Septic children MAY require 200 cc/kg of fluid in the first 24 hours.

  • Tachycardia is the primary mechanism to increase CO in pediatric shock

    • First sign of compensation

  • Don’t forget to place intraosseous access (IO) if unable to establish PIV quickly

  • Most children with community acquired septic shock present in cold shock

  • Children with cold shock likely have cardiogenic dysfunction secondary to sepsis

  • Children who have been appropriately fluid resuscitated AND are refractory to vasopressor should be started on stress dose steroids for secondary adrenal insufficiency. Target fluid resuscitation based on CVP (indirect measure of preload).

Clinical features

Signs: capillary refill, skin turgor, skin temperature, pulse characteristics, hyperdynamic precordium, urine output, altered level of consciousness, increased respiratory effort.

Key management steps

  • Early recognition

  • Rapidly establishing airway and vascular access

  • Rapid fluid resuscitation and evaluate electrolyte and CBC

  • After 60 cc/kg, continue fluid resuscitation if needed and determine need for vasopressors

  • Place Foley, central line, and order PRBCS to keep Hct >30. Set CVP, MAP, UOP goals. If central line is in SVC, check venous saturation.

  • Based on exam and blood pressure initiate either norepinephrine, epinephrine, or milrinone

2. Emergency Management

Stabilizing the patient

  • Rapidly establishing airway, supplemental oxygen, and vascular access

  • Rapid fluid resuscitation and evaluate electrolyte and CBC

  • After 60 cc/kg, continue fluid resuscitation if needed and determine need for vasopressors

  • Place Foley, central line, and order PRBCS to keep Hct >30. Set CVP, MAP, UOP goals. If central line is in SVC, check venous saturation.

  • If unable to place CVL start vasopressors through PIV or IO

  • Based on exam and blood pressure initiate either norepinephrine, epinephrine, or milrinone (see ACCM algorithm).

Algorithm septic shock

Emmanuel Rivers: “Goal Directed Therapy” for Septic Shock

  1. Place CVL to administer vasopressors and measure CVP

  2. Arterial line and establish target blood pressure

  3. Foley: to measure end organ perfusion:

    • UOP 1 cc/kg/hr

  4. Keep Hct 30 to optimize oxygen delivery.

Drugs and dosages

Sodium bicarbonate (milliequivalents) 1-2 meq/kg IV

Dopamine (micrograms/kg/min), max dose pediatrics 20 mcg/kg/min

Norepinephrine (micrograms/kg/min) start 0.05 and go as high as 1 mcg/kg/min

Epinephrine (micrograms/kg/min) start 0.05 and go as high as 1 mcg/kg/min

Milrinone 0.3-1 mcg/kg/min (do not give loading dose)

3. Diagnosis

Establishing the diagnosis

Based on clinical exam a diagnosis of SIRS (See SIRS criteria) and septic shock can be made. Patients are pan cultured and culture results are the only way to determine a specific etiology with a 100% certainty.

Not all patients will have positive cultures.

Clinical presentation and course are enough to make a diagnosis of septic shock.

Often times a specific etiology cannot be found.

Diagnostic approach

After addressing ABCs move onto identifying source for infection and laboratory investigation.

Secondary survey for abscess, cellulitis as an obvious source.

Focused history.

Diagnostic tests

Send blood work CBC, DIC, type and screen (may need to optimize oxygen carrying capacity as pathophysiology evolves), CMP, magnesium, ionized calcium, glucose, phosphorus, lactate, UA, CRP, urine culture, blood culture, respiratory culture, endotracheal tube culture if intubated.

Pay attention particular attention to ionized calcium and glucose in first few minutes of assessing child. Infants higher likelihood of hypoglycemia

Chest radiograph. Additional imagining studies will depend on signs and symptoms (i.e. CT of abdomen or head).

Pathophysiology

Basic equations

Most oxygen is carried by hemoglobin

1. O2 content (CAO2) - [1.34 x HB x Sats] + PaO2 x 0.003

  • Bound

  • Dissolved

2. O2 Delivery (DO2) = Content x cardiac output (CO)

  • CO=HR x SV

  • b.SV:

    • preload

    • afterload

    • inotropy

3. Stroke Volume

  • Preload - the resting length of the myocardium prior to contraction

    • Generally defined by the end of diastolic pressure

    • An increased preload causes increased muscle fiber length → optimized overlap of actin/myosin filaments → increased force of contraction. Too much load on the muscle fibers depresses function

  • Afterload - the impedance against which the heart must pump

    • Mean arterial pressure and systemic vascular resistance

    • Increased afterload impedes emptying of the ventricle and forward flow

  • Contractility - the intrinsic ability to perform work/pump blood and is independent of the loading conditions for the heart

    • Dependent on serum pH, PaO2, glucose, ionized calcium and temperature.

    • Mixed venous oxygen saturation (SvO2) as a measure of cardiac output

      1. SvO2 commonly assumed to represent the mean tissue PO2. Pulmonary arterial sample.

      2. It must be remembered that the SvO2 measures oxygen saturation present in venous drainage of all tissues beds, thus is influenced by relative contributions from tissues with differing metabolic needs.

Septic shock

Patients don’t suddenly decompensate, people suddenly notice.

  1. Early/compensated shock

    • Compensatory mechanisms: Initial tachycardia to maintain CO followed by...

      • Baroreceptor reflexes – small changes in vascular tone and/or vascular pressure. In carotid sinus, aortic arch.

      • Decreased vagal tone, increased HR, decreased coronary resistance, improving myocardial oxygen supply

    • Progresses to increased sympathetic tone, increase in peripheral (skin and muscle bed) vasoconstriction, increasing circulating blood volume

    • Chemoreceptors – located in tissue beds and sense hypoxia and decreased blood flow

      • Results in further vasoconstriction and respiratory stimulation

      • Cerebral ischemia – Most sensitive mechanism.

        1. Cerebral perfusion pressure < 40 mm Hg strongly activates the sympathoadrenal system.

    • Sympathoadrenal system

      • Reabsorption of tissue fluids --> decreased mean arterial pressure and increased arteriolar constriction -->decreased capillary venous pressure. Osmotic pressure becomes greater than hydrostatic pressure, reabsorption of fluids occurs in the capillary beds.

      • Release of endogenous vasoconstrictors – including epinephrine/norepi from the adrenal medulla; vasopressin (ADH) from the posterior pituitary; renin from the kidney

    • Renal conservation of water by the release of aldosterone stimulated by vasopressin causes sodium reabsorption in the renal distal tubule and water follows.

  2. Disease process progresses and CO no longer be maintained while the blood pressure is maintained by increased systemic vascular resistance.

    • Blood flow to the brain, heart, and respiratory muscles is protected at the expense of flow to the skin, skeletal muscle and splanchnic/renal beds.

    • Laboratory data: Metabolic acidosis but a normal to high pH due to respiratory compensation

  3. Late/uncompensated shock

    • A decompensated state where progressive circulatory impairment occurs.

      • Cellular function will deteriorate and lead to vital organ damage.

      • pH begins to fall

      • Hypotension is seen with cyanotic, cold extremities

      • Respiratory distress with grunting and tachypnea/hyperpnea

      • Organ dysfunction becomes apparent with impaired level of consciousness leading to coma

      • Anuria, coagulopathy, ischemic myocardial damage, respiratory failure

    • Laboratory data: Uncompensated metabolic acidosis with low pH. Lab abnormalities indicating organ injury.

    • Clinical status characterized by profound hypotension, falling respiratory effort and rate, tachycardia, which slows to a bradycardic rate heralding impending arrest.

Epidemiology

Sepsis is a leading cause of death in infants and children, with >42,000 cases of severe sepsis annually in the United States and millions worldwide. 50% of the children with severe sepsis in the United States are infants, and half of these infants are low- or very low-birth-weight babies. National hospital costs associated with severe sepsis in the United States were $2.3 billion in 1999. Mortality rates are approximately 10% in children. Children with chronic medical illnesses have higher mortality.

Special considerations for nursing and allied health professionals.

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What's the evidence?

Brierly, J. "American College of Critical Care Medicine clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock*". Crit Care Med. vol. 37. 2009. pp. 666-688.

(This reference is the standard for management of pediatric shock and provides an excellent evidenced based algorithm.)

Rivers, E, Nguyen, B, Havstad, S. "Early goal-directed therapy in the treatment of severe sepsis and septic shock". N Engl J Med. vol. 345. 2001. pp. 1368-77.

(This reference introduces to physicians the concept of settings goals for key parameters in septic shock and demonstrates that this approach reaching target goals improves outcomes significantly in septic shock.)

Watson, RS, Carcillo, JA. "Scope and epidemiology of pediatric sepsis". Pediatr Crit Care Med. vol. 6. 2005 May. pp. S3-5.

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