Hemorrhage is often a major component of traumatic brain injury (TBI). Red blood cells (RBCs), accumulated at the hemorrhagic site, undergo hemolysis upon energy depletion. Hemolysis of RBCs is expected to release free iron into the central nervous system (CNS) which must be managed to prevent iron neurotoxicity. Here, we examine the hypothesis that chronic alcohol consumption, as a secondary stressor, may increase iron toxicity in a rat model of TBI by altering the iron management pathways. We found large accumulations of free iron at the site of hemorrhage with evidence of hemolytic activity. Our observations demonstrate that alcohol use can alter the three distinct iron management pathways: transferrin/hemosiderin binding, lipocalin 2/heme oxygenase 1/ferritin system, and possible microglial phagocytosis. Presence of alcohol prolonged the expression of lipocalin 2 as well as increased and sustained levels of ferritin, while the combined effects of alcohol and TBI elevated the levels of heme oxygenase 1 faster than TBI alone. The hippocampus, neocortex, ventricles, and around vessels near the site of impact appeared to be the prominent brain regions of induction. In addition, we provide evidence that microglia my also play a role in iron management through RBC phagocytosis.