Cerebrovascular complications are rare following a Viperidae snake envenomation, let alone ischemic ones. This catastrophic hemorrhaging cascade is widely known to cause a wide array of manifestations. Its manifestations can range from skin bleeds to fatal intracranial or organ hemorrhages. Our patient had cortical blindness secondary to an ischemic occipital infarct following a hemotoxic snakebite - a seemingly distinct oxymoron. The physician should be mindful of the fact that a hemotoxic snakebite can deceptively bring in ischemic attacks as well. Toxic vasculitis, thrombotic angiopathies, widespread vasospasm and endothelial damage are believed to shoulder a part of the disease process that can bring about tissue ischemia. Key Messages Hemotoxic snake envenomation can have devastating effects. Apart from dealing with the threat of coagulopathy, the physician must also be alert to the ironical ischemic aftermath that can equally bring in misery. Our patient had one such complication-bilateral cortical blindness resulting from bilateral occipital ischemic infarcts. The physician must be aware that a hemotoxic snakebite can even instigate ischemic dilemmas, i.e. cerebrovascular infarcts, as well. How to cite this article Kodiatte Abraham A, Livingston J. Hemotoxic Snakebite Presenting with Bilateral Blindness Due to Ischemic Occipital Infarcts. Indian J of Crit Care Med 2019;23(2): 99-101.

This otherwise fit and well 25 year old gentleman presented with new onset intermittent stabbing headaches associated with generalised tiredness and one nocturnal seizure. His neurological examination was normal and there were no dysmorphic features. He continues to remain intact neurologically.Initial CT Brain showed periventricular low attenuation changes bilaterally associated with bi-frontal atrophy. MRI Brain confirmed extensive periventricular White Matter T2 high signal changes in keeping with Leukomalacia and generalised cerebral atrophy.Genetic testing revealed 2 variant mutations in the EIF2B1 gene, of which one has been previously reported pathogenic and the other is a frame shift variant – likely pathogenic consistent with a diagnosis of vanishing White Matter Leukodystrophy.VWM leukodystrophy is an autosomal recessive disorder characterized by variable neurologic features, including progressive cerebellar ataxia, spasticity, and cognitive impairment associated with WM lesions on brain imaging. The prevalence is unknown; and age at onset can range from early infancy to adulthood. Rapid neurological deterioration can occur following minor head trauma, infections and stress. Mutations in EIF2B1, EIF2B2, EIF2B3, EIF2B4 and EIF2B5 genes cause leukoencephalopathy with Vanishing White Matter.