Early and aggressive intervention is crucial in the management of shock; the longer the shock persists before the start of resuscitation, the worse the outcome. Intervention strategies for shock are twofold. Restore oxygen delivery to the tissues by optimizing oxygen content of the blood.13 Improve tissue perfusion by improving volume and distribution of cardiac output.13
Oxygen content is influenced by oxygen-carrying capacity (hemoglobin) and percent of hemoglobin that is saturated with oxygen (O2 saturation). Administration of 100% oxygen increases bound and dissolved oxygen in the blood. Provide a secure airway via intubation if necessary. With intubation and pharmacologic paralysis, the work of breathing is reduced while simultaneously decreasing oxygen demand. Etomidate is not recommended for children with septic shock as it was associated with increased severity of illness and mortality in adults and children.14 Improving ventilation/perfusion (V/Q) abnormalities using continuous positive airway pressure (CPAP) and positive end expiratory pressure (PEEP) helps to correct V/Q abnormalities.12 Correction of anemia can dramatically increase oxygen-carrying capacity. Less often considered but causes of reduced oxygen delivery are abnormal hemoglobin states from carbon monoxide and nitrites exposure creating carboxyhemoglobin and methemoglobin, respectively.13 Also consider toxins that induce cellular hypoxia despite adequate oxygenation supply—cyanide and hydrogen sulfide exposure.13
In most cases, fluid resuscitation is critical to improving cardiac output. The only contraindication to aggressive fluid management is congestive heart failure. Dehydration and the maldistribution of blood volume can create challenges for vascular access. If intravenous access is difficult, early establishment of intraosseous access is encouraged.15 Current research does not favor colloid over crystalloid fluids for shock resuscitation5 unless septic shock is caused by malaria where colloid is superior to crystalloid in reducing mortality.16,17 Furthermore, provided there is no hepatomegaly or rales to suggest heart failure, rapid and successive 20 cm3/kg boluses of fluid up to 60 cm3/kg or more are warranted until perfusion is restored. In severe sepsis, persistent capillary leak from the systemic inflammatory response syndrome (SIRS) can result in persistent maldistribution of blood volume and significant pulmonary edema. If blood loss is the etiology of shock, it is sensible to replenish the vascular space with blood, as two goals will be accomplished: restoration of intravascular volume and increased oxygen-carrying capacity of the circulating blood volume.
In septic shock, the speed and effectiveness of therapy influences the outcome.5 The preferred emergency strategy of adult septic shock is early goal-directed therapy; this included monitoring central mixed venous oxygen saturation (>70%), mean arterial pressure (>65 mm Hg), CVP (between 8 and 12 mm Hg), and hematocrit (>30%).18 Studies in pediatrics are limited but two studies11,12 support early goal-directed therapy for septic shock in children; perfusion represented by capillary-refill was used as a surrogate marker for cardiac output.
An international consortium developed guidelines for the management of severe sepsis and septic shock in adult and pediatric patients which was updated in 2008.19,20 A proposed approach to pediatric septic shock is referenced in Figure 19-2.5 Therapeutic end-points of resuscitation for septic shock include normalization of heart rate, capillary refill <2 seconds, normal pulses, warm extremities, urine output >1 cm3/kg/h, and normal mental status. Other goal-directed management of pediatric shock is referenced in Figure 19-3.2 Implementation of these guidelines have achieved best practice outcomes with reduction of fluid-refractory shock of 28-day mortality to 3% and hospital mortality of 6%.21
Goal-directed management of pediatric shock.
Early institution of peripheral inotrope delivery is recommended because mortality increased with delay in time to inotrope drug use.14 In both adults18 and children,22 goal-directed therapy of central venous saturations >70% significantly reduced mortality. Sedation and mechanical ventilation provides support for circulation as 40% of cardiac output may be required to support work of breathing. Sedation facilitates hemodynamic monitoring temperature control and reduces oxygen consumption.14 Hydrocortisone therapy should be reserved for use in children with recent steroid therapies, pituitary or adrenal abnormalities, septic shock and purpura, or proven adrenal insufficiency.14 Recombinant human activated protein C (rh-APC) is not recommended in children since this was associated with an increased risk of bleeding and amputations with no reduction in mortality.23
Anaphylactic shock has the potential for airway obstruction due to swelling of the upper airway, so early airway intervention may be warranted. Epinephrine and oxygen are the most important therapeutic agents administered in anaphylaxis. Fluid resuscitation is needed to compensate for the vasodilation related to histamine release. Epinephrine (1:1000) administration intramuscularly to the anterolateral thigh is critical to decreasing morbidity and mortality and is superior to subcutaneous or intramuscular deltoid administration.24 Epinephrine promotes vasoconstriction and decreases mucosal edema through α1 effects. In addition, epinephrine increases heart rate and strength of contractility through β effects along with bronchodilation and stabilization of histamine-releasing mast cells and basophils.8 Repeated doses may be needed and when hypotension is persistent an epinephrine drip (1:10,000) should be started. Other adjunctive therapies include corticosteroids, H1 and H2 blockers, and nebulized albuterol. Patients on β-blockers show decreased effectiveness of epinephrine during anaphylactic episodes.25 In these patients, glucagon may reverse refractory bronchospasm and hypotension. Recommended dose in children is 20 to 30 μg/kg.
Neurogenic shock results primarily through loss of sympathetic innervation from the central nervous system. The hypotension from the loss of vasomotor tone is not always responsive to fluid administration, but does respond to α1 stimulation from norepinephrine and epinephrine.13 Warming measures may be needed since the vasodilation increases insensible heat loss. Bradycardia from loss of sympathetic input to the heart can be improved with epinephrine.
Cardiogenic shock requires therapies that increase the contractility of the heart while reducing the resistance that the heart is working against. Overzealous fluid administration can worsen cardiac function and pulmonary edema. Sedation, pain control, paralysis, and intubation can reduce oxygen demand. Reduction of systemic vascular resistance allows for increases in stroke volume and thus cardiac output. Buffering metabolic acidosis with bicarbonate is thought to improve the myocardial depression that occurs when the pH is less than 7.2.26 Furosemide can be used to treat volume overload. Consultation with pediatric critical care and cardiology should be initiated at the earliest opportunity.
Physical obstructions that impede cardiac output such as tension pneumothorax and cardiac tamponade can be improved with needle thoracentesis and pericardiocentesis, respectively. For those congenital left-ventricular outflow tract lesions that are dependent on the ductus arteriosus for systemic perfusion, continuous prostaglandin E1 infusion restores patency of the ductus by vasodilation.13 Other interventions include ventilatory support, inotropic agents to improve contractility, echocardiography to direct therapy, and correction of metabolic abnormalities (acidosis, hypocalcemia, and hypoglycemia) that impair cardiac function. Pulmonary embolism is rare in the pediatric population unless risk factors are present. Therapy primarily revolves around anticoagulation with heparin and early consultation with pediatric critical care and hematology.