Cerebrovascular complications of cancer

Fernando Testai MD PhD (

Dr. Testai of The University of Illinois College of Medicine has no relevant financial relationship to disclose.

)
Sarah Mufti MD (

Dr. Mufti of the University of Illinois College of Medicine at Chicago has no relevant financial relationships to disclose.

)
Rimas V Lukas MD, editor. (

Dr. Lukas of Northwestern University Feinberg School of Medicine received honorariums from AbbVie and Novocure for speaking engagements, from Eisai for consulting work, and from Monetris as an advisory board member.

)
Originally released September 7, 1994; last updated September 1, 2020; expires September 1, 2023

Overview

Cerebrovascular disease (sinus thrombosis, cerebral infarction, or hemorrhage) is a common complication of cancer and cancer therapy. The management of these vascular disorders in this complex patient population can be challenging. In addition, there have been anecdotal reports of a subset of vascular disorders unique to the cancer patient, including radiation-induced carotid artery atherosclerosis and chemotherapy-induced vasculopathy. In this article, the authors review the clinical milieu in which these disorders develop, and they summarize the pathogenesis, characteristics, and methods of diagnosis of cancer-associated stroke.

Key points

 

• Cancer is a hypercoagulable state leading to an increased risk of venous and arterial thromboembolic events.

 

• Cancer therapies such as radiation and chemotherapy have direct effects on the CNS vasculature.

 

• Patients with cancer are also at risk for intracranial hemorrhage from a variety of factors including thrombocytopenia, coagulopathy, hemorrhagic brain metastases, and hematologic malignancies.

Historical note and terminology

In the mid-1800s, Armand Trousseau first drew attention to the clinical association between thrombophlebitis and cancer. Subsequently, clinicians observed that thrombophlebitis is only one manifestation of cancer-associated coagulopathy, which represents a disruption of the delicate balance that normally exists between hemostatic and fibrinolytic pathways. This coagulopathy is poorly understood and, as discussed below, does not constitute a unique entity (Khorana et al 2005; Khorana et al 2013). Disseminated intravascular coagulation is generally defined as excess thrombin generation within the vasculature that overwhelms normal regulatory hemostatic mechanisms. This results in increased consumption of platelets, coagulation factors, and sometimes inhibitors of coagulation. Defibrination syndrome and consumption coagulopathy are alternate terms for disseminated intravascular coagulation.

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