IVIg Infusion May Be Complicated by Ischemic Stroke
Abstracts & Commentary
Sources: Caress JB, et al. The clinical features of 16 cases of stroke associated with administration of IVIg. Neurology. 2003;60:1822-1824; Okuda D, et al. Arterial thrombosis induced by IVIg and its treatment with tPA. Neurology. 2003;60:1825-1826.
Intravenous immunoglobulin (IVIg) is an effective treatment for a wide range of autoimmune neurological disorders such as Guillain-Barré syndrome, myasthenia gravis, and immune mediated neuropathies. IVIg is well tolerated in general but may rarely result in anaphylaxis and acute renal failure, as well as thromboembolic complications such as pulmonary embolism and stroke. These recent reports in Neurology highlight the potential vascular consequences of IVIg.
Caress and associates report on 16 cases of stroke over a 4-year period at a single medical center. Fifteen of the 16 cases had one or more stroke risk factors, including hematologic disorders such as idiopathic thrombocytopenic purpura (ITP). The majority of strokes (88%) occurred within 24 hours of IVIg infusion. A total of 498 patients during the study period were treated with IVIg, for an overall incidence rate of 0.6%. Risk factors for atherosclerotic disease such as HTN or DM were common. Four of the cases had bilateral infarcts in multiple vascular territories suggesting a diffuse vasculopathy or a shower of emboli.
Okuda and colleagues report on 4 patients with vascular complications of IVIg, 3 of whom were treated with tPA. Three patients had cerebral ischemia and one had a popliteal thrombosis. All 3 patients treated with tPA returned to normal. Serum viscosity was measured to be elevated in one patient. The overall incidence of vascular complications was 4/520 patient days (0.08%); however, the per patient rate was much higher (7%, 4/57).
Commentary
In the absence of randomized data, it is difficult to ascertain the precise stroke risk associated with IVIg. In my personal experience as a stroke specialist, I have seen only 2 cases. Risk is likely increased with higher IVIg concentrations (10% vs 5%) and faster infusion rates, but the reports of Caress and Okuda do not particularly support this. The most likely mechanism of IVIg-related stroke is increased serum viscosity, which is otherwise well tolerated in healthy people. In the presence of risk factors such as established atherosclerotic disease, however, an impaired microvasculature may be unable to accommodate these fluctuations. The presence of preexisting hypergammaglobulinemia in patients with inflammatory syndromes may further compound these viscosity effects.
The use of IVIg is constantly expanding, which includes its use in situations for which there may not be extensive randomized data. In these cases, IVIg therapy might be reconsidered for patients with risk factors who may already be at increased stroke risk. Finally, the excellent tPA outcomes as reported by Okuda et al suggest that although thrombosis may not be the primary mechanism of these strokes, thrombolysis should nevertheless be considered for patients within the appropriate time window. — Alan Z. Segal, MD, Assistant Professor, Department of Neurology, Weill-Cornell Medical College, Attending Neurologist, New York Presbyterian Hospital, Assistant Editor, Neurology Alert.
Intravenous immunoglobulin (IVIg) is an effective treatment for a wide range of autoimmune neurological disorders. IVIg is well tolerated in general but may rarely result in anaphylaxis and acute renal failure, as well as thromboembolic complications such as pulmonary embolism and stroke. These recent reports in Neurology highlight the potential vascular consequences of IVIg.
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