Introduction
SARS Cov-2 infection is a pandemic that continues to ravage the world [1]. The list of its complications continues to grow every day.
Case presentation
We report the case of a young patient admitted to intensive care for limbic encephalitis associated with severely COVID-19 infection.
Discussion
With the COVID-19 outbreak being a global pandemic, various neurological manifestations have been reported [2]. On the other hand, diverse cases of limbic encephalitis related to COVID-19 have been recently described, they are related either to hyper inflammation syndrome with massive release of inflammatory cytokines or to secondary autoimmune response [3].
Conclusion
Seriously ill COVID-19 patients are at a higher risk of limbic encephalitis. It is therefore important to monitor Neurological Events in COVID-19 patients. This makes it possible to start the appropriate treatments quickly and avoid complications.
Introduction
Sars-CoV-2 induces an intense cytokine response called cytokine storm at the origin of acute respiratory distress syndrome, multiple organ dysfunction syndrome and death. In this context, several treatments have been proposed; and plasmapheresis appears as a promising treatment.
Case presentation
We report the case of a 57-year-old patient admitted for Sars-CoV-2 infection, who requiried the use of mechanical ventilation, assistance by veno-venous extracorporeal membrane oxygenation ECMO and treated by plasmapheresis plugged on the ECMO circuit.
Discussion
We discuss the mechanisms responsible for the Sars-CoV-2 induced cytokine storm leading to an acute respiratory distress syndrome and the main therapeutic alternatives with emphasis on plasmapheresis.
Conclusion
Reduction of cytokines by plasmapheresis may be very useful in the management of Covid-19 infection if it is undertaken early even on an ECMO circuit.
Introduction:
Autonomic dysfunction is a prevalent symptom of Guillain–Barré syndrome (GBS); cardiovascular involvement in this scenario has been mentioned infrequently in the literature.
Case Presentation:
A 65-year-old man with GBS presented with reversible left ventricular systolic failure. On first presentation, our patient had no history or indications of heart malfunction. During the clinical manifestation of his autonomic dysfunction, he had electrocardiographic alterations, modestly increased cardiac enzymes, significant left ventricular systolic dysfunction, and segmental wall motion irregularity. Once the initial episode was over, these anomalies and his symptoms resolved quickly.
Discussion:
We believe the reversible left ventricular dysfunction was caused by the toxic impact of elevated catecholamines as well as transiently injured sympathetic nerve endings in the myocardium, which was apparently caused by GBS. We recommend that echocardiography be performed in patients who exhibit clinical signs of autonomic dysfunction, particularly if they are associated with abnormal electrocardiographic findings, cardiac enzyme elevation, or hemodynamic instability, so that appropriate medical therapy can be instituted as soon as possible.
Conclusion:
GBS is a not a very rare situation in our context. Thus, doctors are supposed to know the life-threatening complications such as neurogenic stunned myocardium and be prepared to dodge it.
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