With the exception of occasional splenomegaly, the other abnormal physical findings are those associated with metastatic sites of infection. Toxemia is profound. Purpuric skin and mucosal lesions enlarge rapidly, and extensive intracutaneous hemorrhages may appear. Shock may be associated with a high cardiac output state and an effective decrease in the intravascular volume suggestive of endotoxemia, or it may be accompanied by congestive heart failure and a deterioration of cardiac output. The latter features may reflect myocarditis, which has been noted on histopathologic examination in more than 70 percent of patients with fatal meningococcemia.
Shock is accompanied by disseminated intravascular coagulation of variable severity.
Acute oliguric renal failure and adrenal hemorrhage may also develop, although bilateral adrenal hemorrhage is not the major cause of shock in patients with fulminant meningococcemia. The deleterious effects of endotoxin are mediated through overactivation of host defense mechanisms. Although the syndrome of fulminant septicemia, which produces shock, disseminated intravascular coagulation, adrenal hemorrhage, and purpura fulminans, is most often caused by N. meningitidis , other gram-negative bacteria can produce this condition. In one study, Hemophilus influenzae type b was the etiologic agent in 30 percent of previously healthy children who presented with this clinical picture. When this syndrome occurs in young children, an antibiotic regimen that is effective against both of these organisms should be used as initial therapy.