Botulism is a rare but potentially life-threatening neuroparalytic disease caused by neurotoxins produced by Clostridium botulinum. While the primary clinical focus is on skeletal muscle paralysis, vegetative (autonomic) nervous system involvement significantly contributes to multisystem manifestations, including characteristic changes in skin perfusion, color, and temperature. Autonomic dysfunction in botulism results from the neurotoxin-mediated blockade of acetylcholine release at parasympathetic and sympathetic nerve terminals, leading to dysregulation of sweat glands, cutaneous vasculature, and microcirculation. These changes can manifest as pallor, cyanosis, diaphoresis, or anhidrosis, and may provide early clinical clues to the severity of neurotoxin impact. This review examines the mechanisms by which botulinum toxins interfere with autonomic neural pathways and explores their effects on skin physiology. Literature data indicate that sympathetic overactivity or impairment can lead to local or generalized alterations in cutaneous blood flow, affecting both thermoregulation and barrier function. Furthermore, clinical studies suggest that certain dermatologic signs, such as mottling, flushing, or cold extremities, correlate with systemic autonomic involvement and can serve as adjunctive diagnostic markers in botulism. Management of autonomic-related skin changes in botulism is primarily supportive, focusing on maintaining hemodynamic stability, preventing secondary skin injury, and addressing systemic complications. Early recognition of autonomic symptoms, including dermatologic manifestations, may enhance patient monitoring, guide therapeutic interventions, and improve outcomes.