Hemoadsorption in viscerocutaneous loxoscelism-related multiorgan failure represents a critical area of exploration within modern medicine. Viscerocutaneous loxoscelism, a severe complication of envenomation by Loxosceles spiders (commonly known as recluse spiders), is characterized by systemic inflammation and tissue necrosis that can progress to multiorgan failure. While supportive care remains the mainstay of treatment, hemoadsorption has emerged as a promising therapeutic modality. This essay examines the pathophysiology of viscerocutaneous loxoscelism, the role of hemoadsorption, and its potential to mitigate the progression of multiorgan fail. Loxoscelism results from the bite of Loxosceles spiders, which inject complex venom containing various proteins and enzymes. Among these, sphingomyelinase D is considered the most critical, as it induces dermonecrosis, platelet aggregation, and systemic inflammatory responses. In viscerocutaneous loxoscelism, venom-induced tissue destruction extends beyond the cutaneous site, causing systemic manifestations such as hemolysis, disseminated intravascular coagulation (DIC), and acute kidney injury (AKI). The inflammatory cascade triggered by the venom can lead to a cytokine storm, exacerbating organ dysfunction and increasing mortality risk.
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