Post-COVID-19 Multisystem Inflammatory Syndrome-Related Cerebral Infarction in a Pediatric Patient Managed with Decompressive Craniectomy.

INTRODUCTION: Most people who are infected with the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) are asymptomatic or present with mild upper respiratory symptoms. This is especially true in the pediatric population; however, rarely, a massive cytokine storm can develop, causing multisystem inflammatory syndrome associated with COVID (MIS-C). Furthermore, children may also suffer from acute ischemic strokes secondary to SARS-CoV-2 infection. CASE PRESENTATION: Here, we present a 2-year-old male who was admitted to the hospital with MIS-C and evidence of a previous SARS-CoV-2 infection. On postadmission day 2, the patient was in cardiogenic shock, had acute kidney injury, liver dysfunction, and metabolic acidosis. He had concurrent altered mental status, and his computed tomography scan showed ischemic infarcts in the territory of the right middle cerebral artery and superior cerebellar artery bilaterally. Magnetic resonance angiography confirmed occlusion of the right middle cerebral artery and right superior cerebellar artery. He underwent an emergent decompressive craniectomy due to rapid deterioration and cerebral edema. After the procedure, he continued to improve and was discharged with moderate disability that improved during outpatient rehab. CONCLUSION: Though rare in children, SARS-CoV-2 can lead to AIS, especially in the presence of underlying risk factors such as MIS-C and hypercoagulopathy. AIS can be associated with severe mortality and morbidity; however, even in this severe case of AIS, the patient was successfully treated with a decompressive craniectomy.

On the role of bacterial metalloproteases in COVID-19 associated cytokine storm.

The cytokine release syndrome or cytokine storm, which is the hyper-induction of inflammatory responses has a central role in the mortality rate of COVID-19 and some other viral infections. Interleukin-6 (IL-6) is a key player in the development of cytokine storms. Shedding of interleukin-6 receptor (IL-6Rα) results in the accumulation of soluble interleukin-6 receptors (sIL-6R). Only relatively few cells express membrane-bound IL-6Rα. However, sIL-6R can act on potentially all cells and organs through the ubiquitously expressed gp130, the coreceptor of IL-6Rα. Through this, so-called trans-signaling, IL-6-sIL-6R is a powerful factor in the development of cytokine storms and multiorgan involvement. Some bacteria (e.g., Serratia marcescens, Staphylococcus aureus, Pseudomonas aeruginosa, Listeria monocytogenes), commonly considered to cause co-infections during viral pneumonia, can directly induce the shedding of membrane receptors, including IL-6Rα, or enhance endogenous shedding mechanisms causing the increase of sIL-6R level. Here we hypothesise that bacteria promoting shedding and increase the sIL-6R level can be an important contributing factor for the development of cytokine storms. Therefore, inhibition of IL-6Rα shedding by drastically reducing the number of relevant bacteria may be a critical element in reducing the chance of a cytokine storm. Validation of this hypothesis can support the consideration of the prophylactic use of antibiotics more widely and at an earlier stage of infection to decrease the mortality rate of COVID-19. Video abstract.