Pediatric emergency medicine trisk 3015 3015

There is no consensus for the ideal course of steroids. One regimen used is IV
methylprednisolone at 2 mg/kg/day divided BID for the duration of IV access, with a
transition to oral prednisolone 2 mg/kg/day divided BID. The decision to treat primary
KD with adjunctive agents should be decided in consultation with physicians who have
expertise in managing patients with KD. The use of corticosteroids in refractory KD is
discussed below.
Adjunctive Therapy With Tumor Necrosis Factor Inhibition
Modulation of proinflammatory cytokines, such as TNF-α, has impacted the treatment
of rheumatologic conditions including vasculitis. Elevated levels of TNF-α are
increased in the acute phase of KD. Some recent studies suggest that use of biologic
response modifiers or biologics for adjunctive therapy of primary KD may show
promise. A 2019 retrospective study showed a benefit among a high-risk group of
patients with KD with CAA (z score ≥2.5, but <10) at baseline. Those treated with
corticosteroids or infliximab in addition to IVIG had less progression in CAA size
compared with those treated with IVIG alone. A 2019 double-blind, multicenter trial
using etanercept with IVIG for KD, showed that the use of etanercept appeared to
improve CA dilation in patients who showed baseline abnormalities. However, there
was no significant benefit in IVIG resistance across the entire patient population. More
research is needed in this area. Currently, the data do not support the use of TNF
inhibitors (infliximab and etanercept) as adjuvant therapy for primary KD. The use of
TNF inhibitors in refractory KD is discussed below.
Management of Complications and Emergencies
Cardiovascular. Cardiac abnormalities dominate the pathology of KD. Clinical
examination is often remarkable for tachycardia and gallop rhythms that are more
prominent than expected from the degree of fever and anemia. The EKG in acute KD
may show mild abnormalities consistent with myocarditis, most commonly a prolonged
PR interval and nonspecific ST- and T-wave changes. Echocardiographic evaluation of
myocardial function early in the course of the disease frequently reveals reduced left
ventricular function and contractility. Rarely, myocardial inflammation may progress to
frank CHF. The severity of myocarditis does not correlate with the risk of coronary
artery aneurysms or with other complications such as pericardial effusion, which may

develop during the second week of illness. The effusion rarely progresses to tamponade
and resolves spontaneously in most instances. Valvulitis presenting as either aortic or
mitral regurgitation is rarely seen during the early phases of KD. Late-onset mitral
regurgitation, from papillary muscle dysfunction or myocardial infarction, may also
complicate the clinical course.
Most characteristic of KD is inflammation of the coronary arteries. This progresses
to ectasia or aneurysm formation in 15% to 25% of untreated children. Dilatation of