Objective: Subarachnoid hemorrhage has high mortality and substantial long-term morbidity. Although SARS-CoV-2 infection is associated with hypercoagulopathy, patients may also present subarachnoid hemorrhage. We aimed to synthesize the clinical and paraclinical characteristics, treatment responses, and outcomes of this neurologic complication. Methods: The population included adults and children, and studies investigated patients with subarachnoid hemorrhagein the context of SARS-CoV-2 infection. We included prospective, retrospective, observational, or interventional studies. We systematically reviewed LitCOVID and the COVID-19 WHO database until February 2023, following a published protocol. Results are presented in tabular form to provide a descriptive summary of the findings. Results: We included 107 patients (30 aneurysmal SAH—aSAH, 52 non-aSAH confirmed by vascular imaging, and 25 without vascular imaging). Subarachnoid hemorrhage was concomitant or developed a few weeks after infection. Severity of COVID-19 ranged from asymptomatic (27.8% aSAH, 5.5% non-aSAH) to severe (50% aSAH, 75% non-aSAH). Patients presented inflammatory markers (25% aSAH, 81%non-aSAH), thrombocytopenia (12.5% aSAH, 28.6% non-aSAH), and impaired coagulation (0% aSAH, 28.6% non-aSAH). SARS-CoV-2 reverse transcription-polymerase chain reaction (RT-PCR) in the cerebrospinal fluid was negative in seven patients. Brain samples were positive for SARS-CoV-2 in one case. Conclusions: An inadequate infection response may change aneurysmal size and morphology, with rupture tendency. Renine–angiotensine–aldosteron system disruption with hypertension and cough increases pressure on aneurysmal walls. Furthermore, mycotic and dissecting aneurysms were reported. Non-aSAH accompanies infection-related complications such as cerebral venous sinus thrombosis, reversible cerebral vasoconstriction syndrome, posterior reversible encephalopathy syndrome, or intracerebral hemorrhage. Cytokine release syndrome, endothelial dysfunction, and SARS-CoV-2 affinity for angiotensin-converting enzyme 2 receptors may induce vasculitic processes. Cough precipitates arterial dissection. Hypoxic brain injury, immune thrombocytopenia, and some COVID-19 medications increase bleeding risks.