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Review
. 2023 Mar 30:10:1117214.
doi: 10.3389/fmed.2023.1117214. eCollection 2023.

The effects of ECMO on neurological function recovery of critical patients: A double-edged sword

Jinxia Cai  1   2 , Halidan Abudou  1   2 , Yuansen Chen  1   2 , Haiwang Wang  1   2 , Yiping Wang  1   2 , Wenli Li  1   2 , Duo Li  1   2 , Yanxiang Niu  1   2 , Xin Chen  1   2 , Yanqing Liu  1   2 , Yongmao Li  1   2 , Ziquan Liu  1   2 , Xiangyan Meng  1   2 , Haojun Fan  1   2
Affiliations
Review

The effects of ECMO on neurological function recovery of critical patients: A double-edged sword

Jinxia Cai et al. Front Med (Lausanne). .

Abstract

Extracorporeal membrane oxygenation (ECMO) played an important role in the treatment of patients with critical care such as cardiac arrest (CA) and acute respiratory distress syndrome. ECMO is gradually showing its advantages in terms of speed and effectiveness of circulatory support, as it provides adequate cerebral blood flow (CBF) to the patient and ensures the perfusion of organs. ECMO enhances patient survival and improves their neurological prognosis. However, ECMO-related brain complications are also important because of the high risk of death and the associated poor outcomes. We summarized the reported complications related to ECMO for patients with CA, such as north-south syndrome, hypoxic-ischemic brain injury, cerebral ischemia-reperfusion injury, impaired intracranial vascular autoregulation, embolic stroke, intracranial hemorrhage, and brain death. The exact mechanism of ECMO on the role of brain function is unclear. Here we review the pathophysiological mechanisms associated with ECMO in the protection of neurologic function in recent years, as well as the ECMO-related complications in brain and the means to improve it, to provide ideas for the treatment of brain function protection in CA patients.

Keywords: brain; cardiac arrest; extracorporeal membrane oxygenation; neurologic complications; neuroprotection.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The pathophysiological mechanisms of CA brain injury. The picture represents the morphological changes in brain tissue due to ischaemia and hypoxia following CA, with increased lactic acid, cerebrovascular endothelial damage, increased inflammatory cells, cerebral micro-thrombosis, neuronal damage, dendritic morphological changes, and a range of other pathological processes occurring.
Figure 2
Figure 2
Schematic representation of the cerebral effects of ECMO. The number of brain neurons and nissls was elevated after ECMO resuscitation compared to CA. The number of lactate and d-dimer was decreased after ECMO resuscitation compared to CA. and other inflammatory, metabolic, necrotic, oxidative stress, apoptotic and other cytokine trends are shown in picture.
Figure 3
Figure 3
Diagram of ECMO in combination with other means of neuroprotection. The diagram indicates hemodynamic control, IABP, and EEG utilized during the treatment, respectively. Target temperature management, appropriate gas (H2, CO) interventions, and CRRT can assist in mitigating ECMO-related brain complications and provide ideas for neurological prognosis after ECMO use. TTM, target temperature management; CRRT, continuous renal replacement therapy; IABP, INTRA-aortic balloon pump.
See this image and copyright information in PMC

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