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Subarachnoid hemorrhage (SAH) remains a devastating cerebrovascular emergency with high mortality and long-term neurological morbidity, yet the mechanisms driving secondary brain injury remain incompletely understood. The glymphatic system, a glial-dependent perivascular clearance pathway, promotes convective exchange of cerebrospinal fluid and interstitial fluid through aquaporin-4 water channels on astrocytic endfeet to remove neurotoxic solutes. Emerging evidence implicates glymphatic dysfunction as a key mediator of brain injury after SAH. This review synthesizes current knowledge on the anatomical and physiological foundations of the glymphatic system, examines the multifaceted mechanisms by which SAH disrupts this clearance network, and discusses the pathophysiological consequences linking glymphatic impairment to neurological outcomes. Understanding the glymphatic dimension of SAH pathophysiology may illuminate novel therapeutic targets and ultimately improve the clinical management of this devastating condition.