The goal of shock management is to get oxygen to the tissues and end 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 child 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/hour. Shock treatment varies according to etiology.
The primary means of responding to hypovolemic shock is to provide additional volume. For children, an isotonic crystalloid such as normal saline or Lactated Ringers 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 infants and children. Careful estimates should be made concerning the amount of volume lost (e.g. blood loss), the size of the patient, and the degree of deficit. Current recommendations are to administer 20 ml/kg of fluid as a bolus over 5-10 minutes and repeat as needed.
In 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 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, non-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.)
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.
The management of septic shock is detailed and complex. A full description is beyond the scope of this handbook, though an excellent resource is Brierly et al. 20092 . 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 patients 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.
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 NICU or PICU may be required.
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 patient 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.
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 patients 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 patients with cardiogenic 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.
2 Brierley J, Carcillo JA, Choong K, et al. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. Crit Care Med. Feb 2009;37(2):666-688.