CASE 17846 Published on 17.08.2022

Cerebral Lipiodol Embolism - A rare complication of Transarterial Ethanol Ablation (TEA) for Hepatocellular Carcinoma

Section

Interventional radiology

Case Type

Clinical Cases

Authors

Zi Wei Chua, Kok Beng Loh

Penang General Hospital, Malaysia

Patient

78 years, female

Categories
Area of Interest Head and neck, Interventional vascular, Liver, Neuroradiology brain ; Imaging Technique Head and neck, Neuroradiology brain
Clinical History

A 78-year-old woman with recurrent multifocal hepatocellular carcinoma (HCC) - Child-Pugh Score B, was planned for fifth transarterial ethanol ablation (TEA). During the procedure, the tumours were embolized with 39ml of absolute ethanol: lipiodol (15ml ethanol: 24ml lipiodol) mixture. Post-procedure, she appears delirious and drowsy. A CT brain was performed and suggested features of Cerebral Lipiodol Embolism. Rehabilitation was initiated, and her neurological status improved. Unfortunately, she subsequently deteriorated and succumbed secondary to nosocomial infection.  

Imaging Findings

The first multiphasic contrast-enhanced CT liver of the patient shows a segment VII/VIII arterially enhancing liver mass with wash-out demonstrable in delayed phases, suggestive of hepatocellular carcinoma (Figure 1.1 – 1.4). Subsequently, patient underwent four sessions of transarterial ethanol ablation (TEA) for the segment VII/ VIII liver mass.

The reassessment multiphasic contrast-enhanced CT liver shows multiple new arterially enhancing liver lesions with wash-out in portal venous and delayed phases, suggestive of recurrence (Figures 2.1 and 2.2). The largest new tumour in segment VI, measuring 2.8 x 2.9 x 2.3cm (AP x W x CC)cm.

Hence, decided for the fifth TEA. Pre-ablation angiogram shows multiple tumoral blushes (Figure 3.1). Complete ablation of new segment VI tumours was followed by partial ablation of new segment VII/VIII tumours (Figure 3.2 – 3.3) via selective arterial cannulation and delivery of a total of 39ml of absolute ethanol: lipiodol (15ml ethanol: 24ml lipiodol) mixture.

Post 5th TEA non-contrast-enhanced CT brain shows multiple foci of hyperdensities along the cortical grey-white matter junction, cortical grey matter and deep grey matter of bilateral cerebral hemispheres, suggestive of lipiodol deposition.

Echocardiogram and CT Thorax were not done timely before patient deteriorated and succumbed.

Discussion

Cerebral lipiodol embolism (CLE) is a very rare complication following transarterial chemoembolization (TACE) or transarterial ethanol ablation (TEA). Lipiodol, an ethiodized oil, is an oil-based iodinated contrast agent commonly used for selective hepatic intra-arterial injection for imaging of hepatocellular carcinoma due to its selective retention in arterially enhancing liver tumours. The retention of Lipiodol in hepatocellular carcinoma is attributed to the decrease in Kupffer cells (hepatic macrophages) in tumour tissue and siphoning effect of hypervascularization within the tumour [1,2,3]. The iodinated property of Lipiodol allows it to be imaged on radiographs and computed tomography (CT). 

The underlying mechanism of how Lipiodol reaches the cerebral circulation causing embolism, is not established yet. Various theories were discussed, including shunting between systemic vessels and pulmonary vessels, which occurs when the liver tumour is in vicinity or invades the diaphragm or lung [4]. Intracardiac right to left shunt is also a proposed risk factor for CLE as it facilitates the access of Lipiodol to the systemic circulation, increasing the cerebral lipiodol deposition [5]. Besides that, the incidence of cerebral lipiodol embolism (CLE) is usually dose-dependent, as demonstrated when the lipiodol dose is more than 20ml [7]. In another case analysis in 2015, history of multiple TEA/ TACE procedures, right liver lobe lesion are proposed risk factors of CLE [6].  

The mechanism of Lipiodol causing insult to the brain is believed to be similar to fat embolism syndrome, in which the Lipiodol causes vascular occlusion of the cerebral arteries. Common clinical symptoms of CLE are usually non-specific, which include reduction in patient’s Glasgow Coma Scale (GCS), visual disturbances, hemiparetic weakness and respiratory distress [6]. The severity of symptoms depends on the site and amount of Lipiodol deposition. The symptoms onset of CLE is usually acute or immediately post-procedure [7], as demonstrated in our patient who developed drop in mental status immediately (< 1 hour) after TEA. 

Radiological findings for cerebral lipiodol embolism (CLE) include disseminated hyperdensities which may represent lipiodol deposition in grey matter, grey matter nuclei and grey white matter junction. These lesions may demonstrate hyperintense signals on T2 weighted/ FLAIR sequences and fluid restriction in ADC/ DWI sequences [6]. The mainstay treatment of CLE is supportive and rehabilitative. In a case analysis involving 12 cases of CLE, 8 cases recovered with no neurological deficits within six weeks of supportive therapy, and 3 cases progressed to death [7]. Based on a recent literature review, it was found that older age and female gender carries a worse prognosis comparatively [8].

Differential Diagnosis List
Cerebral Lipiodol Embolism
Hemorrhagic cerebral metastases
Calcified cerebral metastases
Fahr disease
Mineralizing microangiopathy
Final Diagnosis
Cerebral Lipiodol Embolism
Case information
URL: https://www.eurorad.org/case/17846
DOI: 10.35100/eurorad/case.17846
ISSN: 1563-4086
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