Journal of Neurology |
© Springer-Verlag 2009 |
10.1007/s066-x |
Открытое письмо редактору «Неврологического журнала» (Официальный вестник Европейского Неврологического Общества ) от ряда греческих специалистов. В письме описывается несколько случаев жировой эмболии сосудов головного мозга, явившейся осложнением процедуры масляной химиоэмболизации печени.
Теги: масляная химиоэмболизация – осложнения – тромбоэмболия – Греция – 2009.
Letter to the Editor
Lipiodol brain embolism during hepatic transcatheter arterial chemoembolization
Theodoros Karapanayiotides1 
, John Goulis2, Anthi Theodorou2, Athanasia Anastasiou3, Georgios Georgiadis1 and Georgios Ilonidis2
(1) | Department of Neurology, Hippokrateion Hospital, 50, Aigaiou Str., 551 33 Thessaloniki, Greece |
(2) | Fourth Department of Internal Medicine, Hippokrateion Hospital, Thessaloniki, Greece |
(3) | Department of Radiology, Hippokrateion Hospital, Thessaloniki, Greece |
| Theodoros Karapanayiotides |
Received: 3 December 2008 Revised: 3 February 2009 Accepted: 4 February 2009 Published online: 1 March 2009
Without Abstract
Sir,
Transcatheter arterial chemoembolization (TACE) for advanced hepatocellular carcinoma, i. e., the injection of a mixture of iodized oil (lipiodol) and a chemotherapeutic via the tumor feeding artery, hitherto has been complicated by lipiodol brain embolism (LBE) in a few cases [1–5]. Only two of these patients had repeat MRI that documented extensive reversion of the initial DWI abnormalities [5]. We present a case of TACE-associated LBE that demonstrated near-complete resolution of DWI lesions suggesting cytotoxic edema.
During his fourth course of TACE, a 71-year-old man with advanced hepatocellular carcinoma presented a modest monoparesis of the right arm along with transient dysarthria and dizziness. CT scan immediately after the procedure showed multiple infra - and supratentorial brain lesions consistent with the deposition of iodized oil. Three hours later, MRI disclosed multiple nonenhancing cortical and subcortical hyperintense lesions, which represented areas of decreased diffusion on DWI. In particular, the magnitude of ADC decrease in the lesioned areas ranged roughly between 15 and 25% compared to contralateral normal-appearing brain tissue. The patient recovered completely over the following 48 h. A repeat MRI after 1 month documented near-complete resolution of the lesions (Fig. 1).
Fig. 1 CT immediately post-TACE shows extensive hyperdensities involving the cerebellar hemispheres (a) and the convexity of the cerebrum (b, c). In MRI (FLAIR), these lesions appear hyperintense and involve mainly cortical and subcortical watershed areas (d–f). In DWI (b = 1,000) the lesions are hyperintense (g–i) and characterized by low ADC (j–l; arrows indicate corresponding areas in DWI and ADC maps). One month later, repeat FLAIR sequence is almost normal
Hyperintense DWI lesions that exhibit low ADC values are typically suggestive of cytotoxic edema in a setting of acute brain ischemia. Although ischemia-associated DWI hyperintensities can be reversible to a certain extent, it is remarkable that in a setting of both cerebral fat [6, 7] and LBE post-TACE [5], widespread areas of presumed cytotoxic edema have been reported not to evolve to complete infarction (established T2 or FLAIR lesions). To the best of our knowledge, such an extensive reversal of DWI abnormalities has not been reported in acute ischemic stroke. A possible explanation would be that what looks like cytotoxic edema in DWI is actually an overestimation of the true extent of the lesion or a cytotoxic edema “mimic.” A MRI spectroscopy study [6] has suggested that soon after fat embolism, areas of restricted diffusion may simply reflect the presence of large quantities of “sluggish” lipids compared to water. However, secondary ischemia [6] or a neurotoxic effect of free fatty acids [7] may occur later if the embolic material is not rapidly cleared from the brain circulation. This would also explain the “preference” of the lipid emboli and of the associated permanent lesions for the watershed areas of the brain where a slow blood flow cannot be compensated quickly and adequately by collaterals. In our patient, fast clearance of the lipid burden may account for the rapid clinical recovery and the reversion of DWI abnormalities.
Concerning the etiology of brain embolism in patients undergoing TACE, right-to-left shunt (either via a patent foramen ovale or intrapulmonary arteriovenous shunts), shunt from the inferior phrenic artery to the pulmonary vasculature, and an increased dose of infused lipiodol are commonly advocated [1–4]. However, the passage of oil microemboli through the hepatic sinusoids to the pulmonary capillaries and thereafter to the systemic circulation may constitute an alternate pathway [5]. Our patient was investigated only with transthoracic echocardiography that was unremarkable.
References
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2. | Matsumoto K, Nojiri J, Takase Y et al (2007) Cerebral lipiodol embolism: a complication of transcatheter arterial chemoembolization for hepatocellular carcinoma. Cardiovasc Intervent Radiol 30:512–514. doi:10.1007/s092-x |
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