Secondary hemophagocytic syndrome (HPS), also known as hemophagocytic histiocytosis (HLH), is a macrophage proliferative disease with multi-organ and multi-system involvement and progressive exacerbation with immune dysfunction, with an aggressive course and high mortality rate. The main triggering factor is viral infection (68.8%), mainly herpes virus. The mechanism of occurrence is mainly due to the proliferation and hyperactivation of T lymphocytes and macrophages resulting in the release of a large number of inflammatory cytokines such as TNF, IL-1 and IL-6 in a waterfall fashion, which leads to systemic multisystem immune damage. Clinical manifestations may include high fever, hepatosplenic lymph node enlargement, skin and mucosal hemorrhage, rapid liver function deterioration, and central nervous system dysfunction. Laboratory tests may include decreased blood triage, increased liver enzymes, coagulation abnormalities, increased ferritin, impaired NK cell activity, and increased soluble IL-2 receptors. The diagnostic criteria are still based on the 2004 criteria, with 5 out of 8 being met, but the emphasis on the absence of phagocytosis does not exclude the diagnosis of the disease, and spleen and lymph node biopsies have a higher chance of finding phagocytosis than bone marrow biopsies. In terms of treatment, the main focus is to control hypercytokinemia, eliminate its continuous activation of T lymphocytes and macrophages, and reduce the inflammatory storm damage to the organism’s organs, with drugs such as glucocorticoids, cyclosporine A and etoposide (VP16), which is the key drug for treatment, inhibiting the monocyte macrophage system and suppressing viral replication. At the same time, symptomatic treatment can be given according to the different triggers.