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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