Recognizing Shock

Shock is defined as a condition in which peripheral tissues and end organs do not receive adequate oxygen and nutrients. While it is sometimes used interchangeably with severe hypotension, shock does not only occur in the setting of severely low blood pressure. Importantly, the body will attempt to compensate for shock through various mechanisms, most commonly through increased heart rate. The heart rate will increase in an attempt to increase cardiac output (stroke volume x heart rate). Blood flow will be shunted from less vital organs such as the skin to more vital organs, such as the kidneys and the brain. In these cases, the child or the infant may be experiencing shock, but have high, normal, or low-normal blood pressure. This is called compensatory shock and may only persist for minutes to hours before progressing to frank uncompensated shock unless treatment is initiated. Without treatment, these compensatory systems can become overwhelmed and result in the child progressing quickly to critical hypotension and cardiac arrest. Therefore, the simple assessment of blood pressure is not a sufficient way to evaluate potential shock in pediatrics.

Table 18

DISTRIBUTIVE SHOCK

Distributive shock is a condition in which the majority of blood is inappropriately distributed in the vasculature. A common way to conceptualize distributive shock is as a condition in which the vasculature has relaxed and dilated to the point of inadequacy. The arterial blood supply needs to maintain a certain tension in order to maintain blood pressure. Likewise, the venous system must maintain tension as well, so as not to retain too much of the total blood supply. In distributive shock, the blood is not being maintained in the required and needed useful blood vessels. Distributive shock is most commonly caused by sepsis, anaphylaxis, or a neurological problem, all of which cause vascular dilation or loss of blood vessel tone. In distributive shock, the preload, contractility, and afterload vary depending on the etiology.

Table 20

Distributive shock is difficult to recognize because the signs and symptoms vary greatly depending on the etiology. Common symptoms include tachypnea, tachycardia, low to normal blood pressure, decreased urine output, and decreased level of consciousness.

Distributive shock is further categorized into warm and cold shock. If the person is experiencing warm shock, they commonly will have warm, erythematous peripheral skin and a wide pulse pressure in the setting of hypotension. If the person is experiencing cold shock, they commonly will have pale, vasoconstrictive skin and narrow pulse pressure hypotension. In each case, distributive shock is generally considered when the person is likely to have one of the three main causes: sepsis, anaphylaxis, or neurological problem

CARDIOGENIC SHOCK

Cardiogenic shock is caused by inadequate contractility of the heart. One of the key differences between hypovolemic and cardiogenic shock is the work of breathing. In both cases, there will be tachypnea, but in hypovolemic shock the effort of breathing is only mildly increased. However, in cardiogenic shock, the work of breathing is often significantly increased as evidenced by grunts, nasal flaring, and the use of accessory thorax muscles. Also, since the heart is pumping ineffectively, blood remains in the pulmonary vasculature. This causes pulmonary congestion and edema, which can clinically be heard as crackles in the lungs and visualized as jugular vein distension. Pulses are often weak, capillary refill is slow, extremities are cool and cyanotic, and there may be a decrease in the level of consciousness.

OBSTRUCTIVE SHOCK

Obstructive shock is similar to cardiogenic shock in that the impaired heart function is the primary abnormality. In cardiogenic shock, the contractility is impaired; but in obstructive shock, the heart is prevented from contracting appropriately. Common causes of obstructive shock are cardiac tamponade, tension pneumothorax, congenital heart malformations, and pulmonary embolism. Obstructive and cardiogenic shock is most easily distinguished by the contractility of the heart. In obstructive shock, heart contractility is normal, although pumping function is not. Cardiac tamponade is associated with muffled heart sounds since blood is present in the pericardial space. Pulsus paradoxus (e.g. a drop in blood pressure on inspiration) may also be present. Tension pneumothorax is a clinical diagnosis. The trachea may have deviated away from the side of the lesion, and there are absent breath sounds over the affected side of the chest. Consider a pulmonary embolism when the person is cyanotic and/or hypotensive, experiences chest pain, and has respiratory distress without lung pathology or airway obstruction. Risk factors include obesity, hormone use, family history of abnormal clotting, and coagulation factor abnormalities.

Respond to Shock

The goal of shock management is to get oxygen to the tissues and to the organs. This requires having enough oxygen in the blood, getting the blood to the tissues, and keeping the blood within the vasculature. Thus, shock management is dedicated to achieving these three critical goals. In objective terms, this means returning the person to the correct blood pressure and heart rate for their age, restoring normal pulses, capillary refill, and mental status along with a urine output of at least 1 mL/kg an hour. Shock treatment varies according to etiology.

HYPOVOLEMIC SHOCK

The primary means of responding to hypovolemic shock is to provide additional volume. For children, an isotonic crystalloid such as normal saline or Lactated Ringer’s is the preferred fluid for volume resuscitation. While volume repletion is somewhat straightforward in adults, great care must be taken when administering intravenous fluids to children and infants. Careful estimates should be made concerning the amount of volume lost (e.g. blood loss), the size of the person, and the degree of deficit. Current recommendations are to administer 20 mL/kg of fluid as a bolus over 5 to 10 minutes and repeat as needed. In hypovolemic (or hemorrhagic) shock, administer 3 mL of fluid for every 1 mL of estimated blood lost—a 3:1 ratio. If fluid boluses do not improve the signs of hypovolemic, hemorrhagic shock, consider the administration of packed red blood cells without delay. Albumin can also be considered for additional intravenous volume for shock, trauma, and burns as a plasma expander. If fluid boluses do not improve the signs of hypovolemic, hemorrhagic shock, re-evaluation of proper diagnosis and occult blood loss (e.g. into the GI tract) should be considered. The remaining interventions are aimed at restoring electrolyte imbalances (e.g. acid/base, glucose, etc.).

DISTRIBUTIVE SHOCK

The initial management of distributive shock is to increase intravascular volume. The intent is to provide enough volume to overcome the inappropriate redistribution of existing volume. As with hypovolemic shock, administer 20 mL/kg of fluid as a bolus over 5 to 10 minutes and repeat as needed. Beyond initial management, therapy is tailored to the cause of the distributive shock.

Septic Shock

In septic shock, aggressive fluid management is generally necessary. Broad-spectrum intravenous antibiotics are a key intervention and should be administered as soon as possible. In addition, a stress dose of hydrocortisone (especially with adrenal insufficiency) and vasopressors may be needed to support blood pressure. After fluid resuscitation, vasopressors are given if needed and according to the type of septic shock. Normotensive persons are usually given dopamine, warm shock is treated with norepinephrine, and cold shock is treated with epinephrine. Transfusing packed red blood cells to bring hemoglobin above 10 g/dL treats decreased oxygen-carrying capacity. As blood cultures return, focus antibiotic therapy to the particular microbe and its resistance patterns.

Anaphylactic Shock

Intramuscular epinephrine is the first and most important treatment for anaphylactic shock. In severe cases, a second dose of epinephrine may be needed or intravenous administration may be required. Crystalloid fluid can be administered judiciously. Remember that in anaphylactic shock, capillary permeability may increase considerably. Thus, while it is important to support blood pressure overall, there is significant likelihood that third spacing and pulmonary edema will occur. Antihistamines and corticosteroids can also blunt the anaphylactic response. If breathing challenges arise, consider albuterol use to achieve bronchodilation. In very severe cases of anaphylactic shock, a continuous epinephrine infusion in the Neonatal Intensive Care Unit (NICU) or Pediatric Intensive Care Unit (PICU) may be required.

Neurogenic Shock

Neurogenic shock is clinically challenging because often there is limited ability to correct the insult. Injury to the autonomic pathways in the spinal cord results in decreased systemic vascular resistance and hypotension. An inappropriately low pulse or bradycardia is a clinical sign of neurogenic shock. Therefore, treatment is focused on fluids first: 20 mL/kg bolus over 5 to 10 minutes; then reassess the person for a response. If hypotension does not respond to fluid resuscitation, vasopressors are needed. This resuscitation should be done in conjunction with a broader neurological evaluation and treatment plan.

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CARDIOGENIC SHOCK

Since children in cardiogenic shock have a problem with cardiac contractility, the primary goal of therapy is to restore contractility. Unlike most other types of shock, fluid resuscitation is not a primary intervention in cardiogenic shock. Often medications to support contractility and reduce afterload are first-line treatments. In normotensive persons, this means vasodilators and diuretics (both decrease intravascular volume). Contractility is supported with inotropes. Milrinone is often used to decrease peripheral vascular resistance. When additional volume is needed, fluid can be administered slowly and cautiously: 5 to 10 mL/kg over 10 to 20 minutes. A pediatric cardiologist or critical care specialist should manage persons with cardiogenic shock.

OBSTRUCTIVE SHOCK

Causes of obstructive shock require rapid and definitive care since they are acutely life-threatening. Cardiac tamponade requires pericardial drainage. Tension pneumothorax requires needle decompression and subsequent placement of a chest tube (tube thoracotomy). Pediatric heart surgeons can address vascular abnormalities, and ductus arteriosus can be induced to remain open by administering prostaglandin E1 analogs. Pulmonary embolism care is mostly supportive, though trained personnel can administer fibrinolytic and anticoagulant agents. Management of these complex etiologies is beyond the scope of this handbook.