Pediatric sepsis is currently defined as the systemic inflammatory response syndrome (SIRS), which includes either an abnormal temperature or leukocyte count along with tachycardia/bradycardia and/or tachypnea, in the presence of a confirmed or suspected invasive infection Severe sepsis is defined as sepsis plus (1) cardiovascular dysfunction, (2) acute respiratory distress syndrome, or (3) ≥2 organ system dysfunctions Septic shock refers to the subset of patients with cardiovascular dysfunction In 2005, approximately 75,000 children were hospitalized with severe sepsis in the United States at $4.8 billion in health care costs and an estimated mortality of 8.9% Although many patients who appear to have sepsis, severe sepsis, or septic shock have negative cultures, exposure to microbial components (e.g., endotoxin, lipoteichoic acid, viral proteins) is believed to trigger a cascade of inflammatory, coagulation, and vascular mediators that result in severe capillary leak (causing hypovolemia), myocardial depression, and vasomotor instability Although classic septic shock results in hyperdynamic cardiac function and low SVR that manifest as “warm” shock, more than half of children with septic shock exhibit low cardiac output and elevated SVR, or “cold” shock In 2016, Sepsis-3 updated the definition and operational criteria for sepsis and septic shock for adults with sepsis defined as life-threatening organ dysfunction caused by a dysregulated host response to infection and septic shock defined as the subset of sepsis with profound circulatory, cellular, and metabolic abnormalities associated with a greater risk of mortality than sepsis alone These updates acknowledge that SIRS is not always present in sepsis and that cellular/metabolic abnormalities are key components of septic shock Similar revisions to the definition/criteria for pediatric sepsis and septic shock have been proposed but not yet finalized In anaphylaxis, the sudden release of preformed histamine, proteases (tryptase, chymase), and proteoglycans (heparin) in mast cells followed by prostaglandins and leukotrienes leads to the classic symptoms of the skin (urticarial) and respiratory tract (edema, wheezing), as well as a profound vasodilatory response resulting in a low SVR state along with capillary leak causing hypovolemia The resulting neurohumoral response leads to an increase in heart rate and contractility that raise cardiac output (see Chapter 85 Allergic Emergencies ) Neurogenic Shock Neurogenic shock is a special cause of distributive shock resulting from the sudden disruption of sympathetic nerve stimulation to the vascular smooth vessel leading to a profound decrease in SVR Unlike other types of shock, the unopposed vagal activity classically results in bradycardia or, at least, absence of the usual tachycardic response to hypotension Neurogenic shock can be seen