CEREBRAL ANGIOGRAPHIC FINDINGS IN DISSEMINATED INTRAVASCULAR COAGULATION

We have reviewed the clinical and cerebral angiographic findings in 4 patients presenting to our Neurology Service with a fulminating clinical syndrome of acute, multifocal cerebral injury, consistent with multiple cerebral ischemic infarctions with or without a hemorrhagic component. Three had definite, and 1 had presumptive laboratory evidence of disseminated intravascular coagulation.

All showed angiographic changes of acute thromboembolic occlusion of large and medium sized intracranial arteries, involving multiple sites bilaterally, but with predilection for the middle cerebral arteries.

Postmortem examination in 2 cases has confirmed the presence of widespread cerebral and systemic thromboembolism, with both ischemic and hemorrhagic changes in brain and other organs. In both, marantic or nonbacterial endocarditis was found as well, raising the question of whether embolization of the fibrin-platelet aggregates from this lesion could alone account for the findings we described.

We suspect that endocardial involvement may determine the form that the basic syndrome may take, and is always present when cerebral infarction dominates the clinical picture in patients with the DIC syndrome. However, clinical and postmortem evidence of venous involvement in 2 of our patients would suggest in situ vascular deposition of fibrin products as an additional factor in pathogenesis, in some patients at least.

While the angiographic changes described are not pathognomonic for the syndrome of disseminated intravascular coagulation, they are sufficiently distinct from other forms of cerebral vascular disease in their location and distribution to strongly support the clinical diagnosis of this entity. No patient had evidence of pre-existing arteriosclerotic cerebral vascular disease, nor could any other potential site for thromboemboli be found, such as a patent foramen ovale or postinfarction mural thrombus. No element of vasculitis or, for that matter, any other form of primary angiopathy was seen in the tissues studied. Angiographic findings have correlated well with the patient’s neurologic findings, and with neuropathologic findings at postmortem examination.

It has been suggested that the basic pathogenetic mechanism in the syndrome can be arrested by Heparin therapy, but only if diagnosis and treatment are initiated early in the course. When, as in our patients, the syndrome presents with rapidly progressing cerebral involvement, the prognosis will remain poor, unless improved methods of diagnosis permit its recognition within its early stages. We believe that neuroradiographic studies can contribute much toward this goal.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?