Bleeding and Subsequent Anemia: A Precipitant for Cerebral Infarction

Abstract

Background and Objectives: The relationship between bleeding and subsequent anemia (BSA) and the occurrence of stroke has not been sufficiently studied. The purpose of the present study was to elucidate the characteristics of stroke associated with BSA. Methods: We studied 16 consecutive patients with acute stroke associated with anemia (hemoglobin level on admission ≤9.0 g/dl) and compared their stroke subtypes with those of 32 control subjects. Results: The cause of anemia was upper gastrointestinal bleeding in 11 patients (ulcers in 8; carcinomas in 2, and hemorrhagic gastritis in 1), bleeding from a hemorrhoid in 2, uterine cervical bleeding in 1, ecchymosis probably related to medication in 1, and chronic blood drainage in 1. At least 10 patients had a history of recent (<1 week), active bleeding. Clinical and imaging studies showed that all the patients had infarcts and none had intracerebral hemorrhages. Thirteen patients had infarcts in the region of the middle cerebral artery (MCA) (total MCA region in 2; partial, cortical area in 5; subcortical area in 5, and lenticulostriate artery region in 1), 2 had anterior cerebral artery (ACA) region infarction, and 1 had cerebellar infarction. All 11 patients who underwent vascular imaging studies showed significant stenosis and/or occlusion of the internal carotid artery (ICA) (n = 5), the MCA (n = 4), both the ICA and MCA (n = 1), or the ACA (n = 1). Of the different stroke subtypes (large vessel infarction (LVI), small vessel infarction, cardiogenic embolic infarction, intracerebral hemorrhage), LVI was significantly (p < 0.05) more frequent in patients with stroke associated with BSA than in the controls, even though the demographics and risk factors were similar in each group. Conclusions: The close temporal relationship between the bleeding and the onset of stroke, as well as the predominance of the LVI subtype in the BSA-associated group as compared to controls, suggest that BSA may precipitate atherothrombotic cerebral infarction. A hemodynamic alteration, enhanced thrombosis or a combination of these appears to be the pathogenic mechanism.