In a minority of cases, cytokine blockers have been used as a supplemental therapy to inhibit production of IL-6 (tocilizumab) or IL-1 (anakinra); TNF-α-inhibitors (infliximab) have also been used. Inotropic or vasoactive agents are often used for children with cardiac dysfunction and hypotension. Anticoagulants have been used. Low-dose aspirin has been used as an antiplatelet drug.Treatment strategies are being considered to prevent serious long-term complications such as coronary artery aneurysms (the main complication of Kawasaki disease). Close outpatient follow-up by a paediatric cardiology team has been recommended. Causes
While it has been hypothesized that the condition is related to COVID-19, it has also been emphasized that the potential link  "is neither established nor well understood." A temporal association between SARS-CoV-2 infection and clinical presentation of the syndrome is plausible. A causality assessment found that temporality was among the five (out of nine) Bradford Hill criteria that supported a causal relationship between SARS-CoV-2 infection and the development of the syndrome. Further characterization of the syndrome is essential to identify risk factors and help understand causality. It is unclear to what extent this emerging syndrome has a similar aetiology to Kawasaki disease (a condition predating the emergence of SARS-CoV-2, which is currently thought to be triggered by a distinct viral agent). Although some cases resemble toxic shock syndrome, there is no evidence that staphylococcal or streptococcal toxins are involved. The role of comorbidities is unclear. Improved understanding will have potential implications for clinical management. Genome-wide association studies are expected to provide insights on susceptibility and potential biological mechanisms.
Numbers of red blood cells and  platelets may be either normal or decreased. Acute kidney injury and low albumin levels in the blood (hypoalbuminaemia) are common. Low blood sodium levels and raised liver enzymes have been reported. Accumulations of fluid in the lungs (pleural effusion), around the heart (pericardial effusion), and in the abdomen (ascites) have also been reported, consistent with generalized inflammation.Differences with respect to Kawasaki disease include frequent presentation with gastrointestinal symptoms such as vomiting, diarrhoea, and abdominal pain. Neurological involvement also appears to be relatively frequent. It often affects older children, whereas Kawasaki disease usually occurs before the age of five. Multiorgan disease appears to be more frequent. Myocarditis and cardiogenic shock seem to be relatively common. Myocarditis may be more evident in older children and adolescents. Preschool children tend to display more Kawasaki-like characteristics. Features of macrophage activation syndrome appear to be more frequent than in Kawasaki disease. Characteristic laboratory findings that are not usually encountered in Kawasaki disease include very high levels of ventricular natriuretic peptide (a marker of heart failure), as well as somewhat lower platelet counts, lower absolute lymphocyte counts, and higher CRP levels. Very high troponin levels (suggestive of myocardial damage) are also common. Clinical course
Clinical course tends to be more severe than with Kawasaki disease. A childs condition can deteriorate rapidly, even in the presence of reassuring laboratory findings. Many children develop shock and heart failure. Most require paediatric intensive care. Supplemental oxygen is often needed, and mechanical ventilation is sometimes used.