Citation

Gijs J, Lambert J, Meyfroidt G, (2018),
Cerebral microbleeds and intracerebral hemorrhage associated with
veno-venous extracorporeal membrane oxygenation
Acta Neurol Belg. 2018 Jul 6 (epub ahead of print)

Archived version

Author manuscript: the content is identical to the content of the published
paper, but without the final typesetting by the publisher

Published version

http://dx.doi.org/10.10.1007/s13760-018-0975-z

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https://link.springer.com/journal/13760

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greet.vandenberghe@kuleuven.be
+ 32 (0)16 34 40 21
url in Lirias https://lirias.kuleuven.be/handle/123456789/xxxxxx

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Cerebral microbleeds and intracerebral hemorrhage associated
with veno‐venous extracorporeal membrane oxygenation
Jeroen Gijs1 ∙ Julie Lambert2 ∙ Geert Meyfroidt3,4 ∙ Jelle Demeestere1,5,6
 Jelle Demeestere jelle.demeestere@uzleuven.be
1

Department of Neurology, University Hospitals Leuven, Leuven, Belgium

2

Department of Radiology, University Hospitals Leuven, Leuven, Belgium

3

Department of Intensive Care Medicine, University Hospitals Leuven, Leuven, Belgium

4

Laboratory of Intensive Care Medicine, Department
of Cellular and Molecular Medicine, KU Leuven, University of Leuven, Leuven, Belgium

5

Department of Neurosciences, Experimental Neurology, KU Leuven, University of Leuven, Leuven, Belgium

6

Laboratory of Neurobiology, VIB, Center for Brain and Disease Research, Leuven, Belgium

Keywords Cerebral microbleeds ∙ Cerebral microhemorrhages ∙ Extracorporeal membrane oxygenation ∙
Epilepsy ∙ Hemorrhage ∙ Cerebral
A 30‐year‐old woman, 26‐week pregnant, was admitted
to the intensive care unit (ICU) with an influenza‐A
pneumonia and severe acute respiratory distress
syndrome (ARDS). She deteriorated while on protective
lung ventilation, steroids and intermittent proning.
Day 4, an emergency caesarian section was
performed, followed by initiation of venovenous
extracorporeal membrane oxygenation (ECMO).
ECMO was continued for 12 days. She was
extubated 2 days later. 1 week after extubation she
had a tonic–clonic epileptic seizure, treated with
diazepam and levetiracetam. On brain computed
with
tomography (CT), a hyperdense lesion
surrounding edema in the right parietal lobe was seen
(Fig. 1). Magnetic resonance imaging (MRI) showed
multiple microbleeds (MB) at the cortico‐subcortical
junction and deep white matter, and one larger
hemorrhage in the right parietal cortex, which caused
the seizure (Fig. 2). The patient was discharged home
after 1 month and remained seizure free under
levetiracetam 500 mg bd. The baby is still in the neonatal
ICU.
MB are small (< 10 mm), round and hypo‐intense
lesions readily visible on gradient‐recall echo or
susceptibility‐ weighted MRI which are often
invisible on CT [1]. His‐ topathologically, they
correspond to areas of hemosiderin deposition as a
result of prior self‐limiting microhemorrhage usually
secondary to small vessel disease [1]. However, dif‐
fuse MB at the cortico‐subcortical junction and the
corpus callosum have been described in ARDS,
ECMO, anoxic brain injury and high altitude cerebral
edema [2–5], often in patients without small vessel
disease. The pattern of MB seen in ARDS patients on

ECMO is not typically seen in conditions associated
with MB likely caused by sporadic small vessel
disease or thromboembolism, such as cardiac valve
surgery [6]. The pathophysiology is unclear, but (a
combination of) hypoxemia, rapid post‐hypoxic
reoxygenation,
increased
venous
pressure,
thromboembolism and systemic inflammation have
been proposed [2–4, 7, 8]. The corpus callosum and
subcortical U‐fibers are relatively resistant to acute and
chronic ischemia due to a rich vascu‐ lar supply and
vascular anastomoses [9]. In animal models, rapid
reoxygenation after anoxic injury has shown to induce
MB with a predilection for small penetrating blood
vessels without smooth muscle layer, similar to the
vasculature of the corpus callosum [7]. The selective
vulnerability of this specific vascular region remains
unexplained. Larger brain hemorrhages causing focal
symptoms may occur in up to 15% of ECMO‐treated
patients [3]. Although good outcomes are reported in
patients with isolated ECMO‐associated MB, possible
long‐term effects on cognition are not known [4].
Acknowledgements The authors would like to
acknowledge the patient, who consented to the
publication of this manuscript. We would like to thank the
medical and nursing staff of the departments of Inten‐ sive
Care Medicine, Pneumology, and Neurology for their care
to the patient. Prof Meyfroidt is supported by the Research
Foundation, Flan‐ ders (FWO) as senior clinical investigator
(1843118N). Dr Demeestere is supported by a clinical
research and eductional board (KOOR) grant from Leuven
University Hospitals.

Funding No funding was received for this study.
Compliance with ethical standards
Conflict of interest All authors declare that they have
no conflict of interest.
Informed consent Patient informed consent was obtained
Ethical approval Ethical approval was waived given
the anonymous nature of the presented patient data.
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Fig. 1 Computed tomography image, axial slice through the lateral ventricles. The arrow shows a small, hyperdense hemorrhage, juxtacortical
in the right parietal lobe. Perilesional edema is visible as a surrounding hypodense rim

Fig. 2 Gradient echo magnetic resonance images, left to right correspond to axial slices from cranial to caudal through the brain. Microbleeds
are shown as multiple hypo-intense foci of hemosiderin deposition bilaterally. These are most abundant in the juxtacortical white
matter (white arrows in a) and in the corpus callosum (black arrows in b and c). There are also several lesions in the deep white matter
(white arrows in c). A larger, symptomatic hemorrhage is also visible