Early brain injury (EBI) is a series of pathophysiological changes occurring within 72 h after subarachnoid hemorrhage (SAH) and before cerebral vasospasm, which is a key factor affecting the outcome of SAH. The possible pathological mechanisms include cell metabolism, oxidative stress and immune inflammation, in which inflammatory response plays an important role. As the important immune cells in the central nervous system, microglia undergo M1/M2 polarization after brain injury. On the one hand, microglia secrete proinflammatory cytokines through Toll-like receptor 4 (TLR4), calcium sensing receptor (CaSR) and triggering receptor expressed on myoid cells 1 (TREM-1) mediated signaling pathways, which are involved in neuronal apoptosis, blood-brain barrier damage and brain edema after SAH. On the other hand, microglia play the anti-inflammatory and protective effects through the expression of neuroglobin and heme oxygenase 1. This article reviews the M1/M2 polarization process of microglia in EBI after SAH and its dual mechanisms of action.