Redness of the lips and mouth is the initial manifestation of oropharyngeal changes caused by cutaneous mucosal lymph node syndrome. Cutaneous mucosal lymph node syndrome, also known as Kawasaki disease (Kawasakisyndrome), is an acute systemic vasculitis with predominant onset in infants and children. The disease was first reported as cutaneous mucosal lymph node syndrome after cases with characteristic manifestations such as persistent fever, rash, and lymphadenopathy, after which it was then found that Kawasaki disease was not a benign disease and that many children died due to complications of cardiovascular disease; in fact, Kawasaki disease has become one of the two major factors causing acquired cardiovascular disease in children, and in many places its risk is even In fact, Kawasaki disease has become one of the two leading causes of acquired cardiovascular disease in children, and in many places its risk is even greater than that of rheumatic fever. Despite extensive research, the etiology of Kawasaki disease is still unclear, but numerous epidemiological and clinical observations suggest that Kawasaki disease is caused by infection, given the fever, rash, conjunctival congestion, and swollen cervical lymph nodes that characterize this self-limiting disease, as well as the prevalence in children and the marked geographic distribution of outbreaks, suggesting an infection-related pathogenesis. The main pathological changes in Kawasaki disease are vasculitis, which can be divided into 3 stages: 1. Stage I: 0-9 days after onset, the main pathological changes are small vessel vasculitis, with small artery holoprosencephaly and periarteritis of the middle and large arteries common, while whole heart vasculitis can be seen, which is prone to arrhythmia and heart failure, and even cardiogenic shock and death. 2.Stage II: 10-25 days after the onset of disease, microvascular inflammation and cardiac inflammation are reduced during this period, but the middle arteries show pericarditis, most obviously in the coronary arteries, aneurysm and thromboembolism may occur, and death may occur due to severe heart failure, arrhythmia, myocardial infarction and coronary artery aneurysm rupture. 3.Stage III: 28-40 days after onset, although small arteritis and cardiac inflammation subsided during this period, granulation tissue proliferation and significant intimal thickening in the middle arteries, aneurysmal dilatation and thrombosis may occur, and death may occur due to myocardial infarction.