Cerebral fat embolism and carotid thrombosis

Clinical History

A 51-year-old man with pulmonary fibrosis received single lung transplantation from a brain-dead donor who had experienced a cranioencephalic traumatism. In the immediate postoperative period, the patient remained unresponsive after the withdrawal of sedation and showed anisocoria with left midriasis.

Imaging Findings

Brain CT showed early acute right hemispheric (corresponding to the anterior and middle cerebral artery territories) and midbrain infarctions, with diffuse oedema and subfalcine herniation. Hypodense filling defects (-23 Hounsfield units) were observed in the basilar top artery and left posterior cerebral artery (Figure 1). CT angiography was subsequently performed and not only confirmed the fatty lesion in the basilar artery (Figure 2) but also demonstrated a right internal carotid thrombosis and a flap of dissection within the artery lumen (Figure 3).

Discussion

We herein report a case of fatal stroke after lung transplantation, in which two different mechanisms concur: cerebral fat embolism and carotid dissection.
Fat embolism is a rare cause of embolic stroke [1]. It usually occurs in patients with severe traumatisms or bone fractures but only 0.9-2.2% of patients is clinically significant [2, 4]. Fat emboli have also been reported in many other situations, such as cardiopulmonary bypass, aortic clamping, dislodgment of epicardial or pericardial fat, liposuction, acute pancreatitis, propofol infusion, and bone marrow transplant [1, 3].
The classic triad of fat embolism syndrome consists of respiratory distress, altered mental status and petechial rash. However, neurologic symptoms are often transient and can vary from focal deficits to diffuse encephalopathy [1, 4].
Cerebral fat embolism usually consists of multiple microembolic infarctions, with classic starfield pattern on diffusion-weighted MR imaging [4].
In this case, a hypodense filling defect can be seen within the posterior cerebral artery lumen and basilar top artery in the CT-angiogram. This has been previously called as the “hypodense artery sign”, in opposition to the “hyperdense cerebral artery sign”, an early marker of acute stroke in CT [3, 6].
We hypothesize that undiscovered fat pulmonary emboli were transferred from donor to recipient via the transplanted lung. We should keep in mind that transplanted lungs come from brain-dead patients for whom the cause of death is a traumatic in approximately 40% of the cases, so fat embolism may be a potential mechanism for neurological symptoms in these patients [5].
On the other hand, a carotid dissection was also identified in this patient as another mechanism for his neurological deterioration.
Dissections of the arteries of the neck are an uncommon cause of stroke, especially in young patients [7, 8]. Carotid dissections may be categorized as traumatic or spontaneous. Trauma implicated in causing carotid dissection ranges from minor to severe and includes iatrogenic causes. However, it is often difficult to determine whether the dissection is truly spontaneous or results from minor trauma– as it happened in this case–, given that clinical presentation, imaging appearance and pathology findings do not significantly differ [8]. Spontaneous carotid dissection can be associated with minor head and neck traumatisms. Among iatrogenic causes, it has been described in association with general anaesthesia, fine needle aspiration, and cardiac resuscitation [8, 9, 10].
Typical imaging findings of carotid dissections include a long tapered stenosis, luminal flap, false lumen, and dissecting aneurysm, the former being particularly suggestive. [11]

Differential Diagnosis List

Final Diagnosis

Cerebral fat embolism and simultaneous carotid thrombosis.

URL:	https://www.eurorad.org/case/11874
DOI:	10.1594/EURORAD/CASE.11874
ISSN:	1563-4086