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Distributive Shock

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Distributive Shock

The goal of treating distributive shock (secondary to septic, anaphylactic, or neurogenic shock) is to increase intravascular volume. Vasoactive agents may be used if rapid boluses of IV fluid fail to perfuse the patient or if the diastolic pressure decreases, causing a wide pulse pressure.

Pediatric Septic Shock

Short Description

Sepsis is a frequent cause of shock in pediatric patients caused by an infectious agent or an inflammatory stimulus. Septic shock is the most common form of distributive shock, which causes the blood vessels to dilate and increases capillary permeability.

Algorithm at a Glance

  • Assess for signs and symptoms of sepsis
  • Stabilize the child
  • Appropriately administer fluids
  • Appropriately administer medications as needed

Goals for Management

The clinician will be able to:

  • Identify sepsis early 
  • Maintain normal vital signs and oxygen saturation
  • Improve the child’s mental status
  • Improve perfusion

Related Video – Types of Shock


The Pediatric Septic Shock Algorithm

Boxes 1 and 2 are completed within the first 10 to 15 minutes and usually in the emergency department. Boxes 3 through 6 are typically completed in the first hour. Box 7 outlines medication treatment for septic shock.

Pediatric septic shock algorithm.

Pediatric Septic Shock Algorithm

Box 1: Assess for Signs of Septic Shock

Clinical signs of septic shock include fever and increased or decreased white blood cell count with a shift to the left and increased bands and immature WBCs, along with metabolic acidosis, respiratory alkalosis, and the presence of a petechial or purpuric rash. 

The clinician watches for:

  • Altered mental status
  • Change in heart rate (usually tachycardia)
  • Fever or hypothermia
  • Increased capillary refill time
  • Hypotension or normotension
  • Change in peripheral perfusion

Related Video – Pediatric Assessment Triangle


Box 2: Initial Stabilization

Goals at this stage are to normalize vital signs, increase perfusion, and improve mental status. The team follows local protocol, which should include:

  • Monitoring heart rate, blood pressure, oxygen saturation, and waveform capnography to support ABCs
  • Obtaining intravascular access (IV or IO)
  • Administering fluid boluses at the rate of 10–20 mL/kg of an isotonic crystalloid solution, followed by an assessment for respiratory distress; fluid bolus administration is repeated as needed

Box 3: Treatment in the First Hour

Within the first hour, the team:

  • Draws blood for cultures and other lab tests
  • Administers broad-spectrum antibiotics (this step must not be delayed)
  • Administers repeat fluid boluses for continued signs of shock while assessing after each bolus for respiratory distress or hepatomegaly
  • Administers antipyretics for fever
  • Continues to assess for signs of septic shock from Box 1

Important clinicians obtain bacteria cultures.

It’s important clinicians obtain bacteria cultures, as an infectious agent can cause septic shock.

Vancomycin commonly treats septic shock.

Vancomycin is a broad-spectrum antibiotic commonly used to treat septic shock.

Box 4: Persistent Signs of Shock After 40–60 mL/kg Total Fluid?

If the signs of shock do not persist, the provider proceeds to Box 5

If the signs of shock persist, the provider proceeds to Box 6.

Box 5: Signs of Shock Are Relieved

If the child’s signs and symptoms are relieved, the provider considers critical care consultation.

Box 6: Persistent Signs of Shock

If the signs of shock are NOT relieved, the team calls for a critical care consult and administers and titrates either epinephrine or norepinephrine.


Related Video – One Quick Question: What is the Epinephrine & Amiodarone Trick?


Related Video – Epinephrine – ACLS Drugs


Box 7: Continued Treatment

When the initial stabilization is complete, the team:

  • Establishes a central IV line and arterial pressure monitoring
  • Titrates epinephrine or norepinephrine and fluid therapy to treat shock
  • Maintains a patent airway and adequate ventilation and oxygenation
  • Considers hydrocortisone if the hemodynamics are unresponsive to fluids and vasoactive drug treatment

Understanding the Septic Shock Algorithm

Since the primary cause of septic shock is an infection that elicits the hemodynamic and metabolic changes, most likely from the activation of inflammatory mediators, the clinician must treat the infection by providing the appropriate antibiotics. However, the goal of immediate shock management is to stabilize the hemodynamic changes and support organ function.

There are three phases in the treatment of septic shock: 

  1. The first phase is the early detection of signs of shock. Children with septic shock may have altered mental status, abnormal heart rate, fever, or poor perfusion. Systolic or diastolic hypotension may be present. 
  2. The second phase is initial stabilization and resuscitation. This phase is the most critical for the survival of the patient. After septic shock is recognized, the patient’s airway and breathing need to be assessed and stabilized as indicated. Cardiac and SpO2 monitoring should be initiated. Vascular access with either an IV or IO line should be obtained within 10 to 15 minutes. 
  • Fluid resuscitation with a 10–20 ml/kg bolus of an isotonic crystalloid solution should be delivered within 10 to 15 minutes of recognizing septic shock. 
    • The child should be reassessed after a bolus and additional boluses repeated as necessary. 
  • Fluid overload during treatment for septic shock increases morbidity rates. 
    • Providers should use their best clinical judgment to determine if fluid boluses should be 10 mL/kg or 20 mL/kg. 
    • If the patient experiences signs and symptoms of pulmonary edema, fluid therapy should be halted. 
  • Antibiotics should be given to the patient within 1 hour. 
    • Antibiotic administration should not be delayed for blood culture results. 
  • The team must correct hypoglycemia or hypocalcemia within the first hour.
  • Lactate concentration, base deficit, and central venous oxygen concentration are indicators of shock severity.
  • Vasopressors should be given for septic shock refractory to fluid therapy within the first hour. 
    • Epinephrine is the first choice of vasopressor medications. 
    • Norepinephrine can be used if epinephrine is not available. 
  • The child should be intubated as necessary to assist ventilation with positive end-expiratory pressure and oxygen supplementation.
  • Consultation from a pediatric intensivist should be obtained.
  1. If shock persists after treatment, the provider seeks expert care and transports the patient to the critical care unit. In the ICU, a central venous line might be established for continuous hemodynamic monitoring and titration of vasoactive drugs to treat the shock. The ICU team must monitor and correct serum electrolytes, acid-base balance, lactate, glucose, and calcium concentrations. The goal of critical care is to achieve a central venous oxygen saturation of 70% or higher, with no signs of shock.

Therapeutic Goals of Vasoactive Agents

The goal of vasoactive therapy in septic shock is to increase ScvO2 to 70% or more. Clinical indicators of improvement include an increase in the cardiac index, normalized heart rate, adequate blood pressure, good distal pulses and perfusion with prompt capillary refill, improved mental status, increased urine output, and normalized metabolic acidosis and lactate concentration.

Correcting Adrenal Insufficiency

Adrenal insufficiency due to the end-organ effects of shock can cause resistance to fluid, epinephrine, or norepinephrine therapy. An IV dose of hydrocortisone (1–2 mg/kg bolus) may be considered for the child refractory to fluid and medication interventions. If time allows, obtaining a baseline serum cortisol before giving hydrocortisone is useful.

Anaphylactic Shock

Anaphylactic shock is an acute life-threatening cause of distributive shock. Treatment emphasizes its effect on cardiopulmonary functions and requires immediate reversal of the mediators that exacerbate the allergic response system. Anaphylactic shock can present with angioedema, which causes tissue swelling. If the upper airway is involved, the patient may need immediate intervention for maintaining an airway and assisting ventilation. 

Anaphylactic shock also causes severe hypotension, and the effects of epinephrine can reverse it. The most critical intervention is to administer epinephrine IM to reverse the effects of histamine, the primary mediator of an allergic response. When necessary, a second dose should be administered 10–15 minutes after the first. A low-dose epinephrine infusion of < 0.05 mcg/kg/minute may be considered if the patient does not respond to initial administration. Hypotension and poor perfusion should be addressed with a fluid bolus of an isotonic crystalloid solution. 

Antihistamines such as diphenhydramine can block the H1 receptors. Ranitidine and famotidine are H2 receptor blockers. The combination of both H1 and H2 receptor blockers is a more effective intervention than giving either class alone. Corticosteroid administration should also be considered.

Albuterol via metered-dose inhaler or nebulizer can be provided to relieve bronchospasm. 

After stabilization, the child should be admitted and monitored for possible late-phase symptoms.

Neurogenic Shock

Children with neurogenic shock will have minimal response to fluid resuscitation because the innervations that produce the compensatory mechanisms are damaged. Therefore, giving fluid therapies to correct hypotension may be ineffective. 

These patients may not be able to autoregulate temperature, which may cause them to be very sensitive to temperature changes. The provider must be ready to give supplementary warming or cooling.

The child with neurogenic shock should be treated with IV fluid therapy with close monitoring of their blood pressure and response to tissue perfusion and oxygenation. Vasopressors may be given if IV bolus fluid therapy is not enough.

Cardiogenic Shock

Myocardial dysfunction is the primary cause of cardiogenic shock. The initial presentation may mimic hypovolemic shock. However, if cardiogenic shock is suspected, treatment should begin with smaller volumes of IV bolus fluid therapy (5–10 mL/kg) given over 10–20 minutes. If the child has not improved after the initial fluid therapy, the provider should conclude that the patient’s condition is due to cardiogenic shock. 

In the case of cardiogenic shock, the provider will see pulmonary edema, respiratory dysfunction that deteriorates, or venous congestion and cardiomegaly following fluid therapy. Patients with venous congestion present with elevated central venous pressure, distended jugular veins, or hepatomegaly

The patient may need central venous access to facilitate the measurement of the central venous pressure, which gives the provider insights into the preload status of the patient. Central venous access also allows for monitoring of central venous oxygen saturation. 

Other necessary diagnostic tests include arterial blood gas, hemoglobin concentration, lactate concentration, ScvO2, cardiac enzymes, and thyroid function tests. Cardiomegaly should be assessed by performing a chest X-ray.

The goal in the management of cardiogenic shock is to improve cardiac output and ejection fraction while controlling the metabolic demands of the patient. Additional fluid therapy is not necessary for cardiogenic shock because these patients already have high preload. To effectively increase the stroke volume, the team must work to decrease SVR. 

Patients may need medications for cardiogenic shock. Vasodilators and diuretics reduce SVR in a normotensive patient. Diuretics also improve pulmonary edema and systemic venous congestion. If it is necessary to increase myocardial contractility, inotropes and inodilators such as phosphodiesterase enzyme inhibitors (e.g., milrinone) may be considered. However, inotropic agents increase metabolic demand and should be avoided unless the patient is hypotensive.   

Another therapy to support the treatment of cardiogenic shock involves decreasing the patient’s metabolic demand by giving ventilatory support and using antipyretics, analgesics, and sedatives. Analgesics and sedatives help to compensate for the low ejection fraction by decreasing stress mediators and, in effect, reducing oxygen consumption and redistributing blood flow to tissues.

Ultimately, the provider must seek to consult with a pediatric cardiologist to help in the management of cardiogenic shock. Extracorporeal life support can be a viable treatment option if the child is at an institution with an experienced cardiologist and staff.

Obstructive Shock

The main treatment for obstructive shock is correcting the obstruction that hinders cardiac output. Therefore, it is a priority to diagnose the cause of obstructive shock immediately because it can rapidly progress into cardiopulmonary failure and cardiac arrest in these patients. 

When managing obstructive shock, a crystalloid solution fluid challenge given at 10–20 mL/kg is an acceptable early intervention while diagnosis and resolution of the underlying cause are in progress.

Obstructive Shock: Causes and Treatment

Causes and treatment for obstructive shock.

Causes and Treatment for Obstructive Shock