Cerebral pseudoinfarction due to venoarterial extracorporeal membrane oxygenation:A case report

BACKGROUND Neurological complications are common in the management of venoarterial extracorporeal membrane oxygenation(VA-ECMO),with most patients requiring sedation and intubation,limiting the assessment of neurological function.Therefore,we must rely on advanced neuroimaging techniques,such as computed tomography angiography(CTA)and computed tomography perfusion(CTP).Because ECMO changes the normal blood flow pattern,it may interfere with the contrast medium in some special cases,leading to artifacts and ultimately misleading clinical decisions.CASE SUMMARY A 61-year-old man presented to a local hospital with chest tightness and pain 1 d prior to presentation.The patient was treated with VA-ECMO after sudden cardiac and respiratory arrest at a local hospital.For further treatment,the patient was transferred to our hospital.The initial consciousness assessment was not clear,and routine CTP was performed to understand the intracranial changes,which suggested a large area of cerebral infarction on the right side;however,the cerebral oxygen was not consistent with the CTP results,and the reexamination of CTA still suggested a right cerebral infarction.To identify this difference,bedside transcranial Doppler was performed,and the blood flow on both sides was different.By reducing the ECMO flow,CTP reexamination showed that the results were normal and consistent with the clinical results.On day 3,the patient was alert and showed good limb movements.CONCLUSION In patients with peripheral VA-ECMO,cerebral perfusion confirmed by CTP and CTA may lead to false cerebral infarction.

Obstructive sleep apnea aggravates neuroinflammation and pyroptosis in early brain injury following subarachnoid hemorrhage via ASC/HIF-1α pathway

Obstructive sleep apnea can worsen the prognosis of subarachnoid hemorrhage.Howeve r,the underlying mechanism remains unclear.In this study,we established a mouse model of subarachnoid hemorrhage using the endovascular perforation method and exposed the mice to intermittent hypoxia for 8 hours daily for 2 consecutive days to simulate sleep apnea.We found that sleep apnea aggravated brain edema,increased hippocampal neuron apoptosis,and worsened neurological function in this mouse model of subarachnoid hemorrhage.Then,we established an in vitro HT-22 cell model of hemin-induced subarachnoid hemorrhage/intermittent hypoxia and found that the cells died,and lactate dehydrogenase release increased,after 48 hours.We further investigated the underlying mechanism and found that sleep apnea increased the expression of hippocampal neuroinflammatory factors interleukin-1β,interleukin-18,inte rleukin-6,nuclear factorκB,pyro ptosis-related protein caspase-1,pro-caspase-1,and NLRP3,promoted the prolife ration of astrocytes,and increased the expression of hypoxia-inducible factor 1αand apoptosis-associated speck-like protein containing a CARD,which are the key proteins in the hypoxia-inducible factor 1α/apoptosis-associated speck-like protein containing a CARD signaling pathway.We also found that knockdown of hypoxia-inducible factor 1αexpression in vitro greatly reduced the damage to HY22 cells.These findings suggest that sleep apnea aggravates early brain injury after subarachnoid hemorrhage by aggravating neuroinflammation and pyroptosis,at least in part through the hypoxia-inducible factor 1α/apoptosis-associated speck-like protein containing a CARD signaling pathway.