Intracranial Bleeding After Reperfusion Therapy in Acute Ischemic Stroke

Abstract

Intracranial hemorrhage is one of the most feared complications following brain infarct. Ischemic tissues have a natural tendency to bleed. Moreover, the first recanalization trials using intravenous thrombolysis have shown an increase in mild to severe intracranial hemorrhage. Symptomatic intracerebral hemorrhage is strongly associated with poor outcomes and is an important factor in recanalization decisions. Stroke physicians have to weigh the potential benefit of recanalization therapies, first, with different risks of intracranial hemorrhage described in randomized controlled trials, and second with numerous risk markers that have been found to be associated with intracranial hemorrhage in retrospective series. These decisions have become quite complex with different intravenous thrombolytics and mechanical thrombectomy. This review aims to outline some elements of the pathophysiological mechanisms and classifications, describe most of the risk factors identified for each reperfusion therapy, and finally suggest future research directions that could help physicians dealing with these complications.

Keywords: brain hemorrhage; hemorrhagic transformation; intracranial bleeding; intravenous thrombolysis; mechanical thrombectomy; reperfusion; stroke.

Figure 1

(A) Isolated petechia of the posterior part of the lenticular nucleus: Moulin Hi d1, ECASS HI1, Heidelberg HI1, (B) Confluent petechial of the lenticular nucleus: Moulin HI d2, ECASS HI2, Heidelberg HI 2, (C) Cortical parenchymal hemorrhage: Moulin HI c1, ECASS HI1, Heidelberg HI1, (D) Deep parenchymal hemorrhage with mass effect and intraventricular hemorrhage: Moulin IIH d2, ECASS PH2, Heidelberg PH2 + class 3b, (E) isolated subarachnoid hemorrhage: Heidelberg class 3c, (F) Massive parenchymal hematoma Moulin IIH d2, ECASS, and Heidelberg PH2.

Figure 2

Massive cortical hemorrhage with mass effect mostly caused by the infarcted tissue, which could be classified as Moulin HI c2, ECASS HI2, or Heidelberg HI2.