Background and Aims: Pneumopericardium is a rare air leak syndrome caused by the abnormal presence of air in the pericardial sac, with a high risk of morbidity and mortality. It is clinically divided into nontension and tension pneumopericardium, with the latter resulting in a decreased cardiac output and circulatory failure. There are limited data regarding nontraumatic pneumopericardium in nonventilated pediatric patients. Therefore, we aimed to describe a case of tension pneumopericardium and review the available literature. Methods: Case report and literature review of nontraumatic pneumopericardium in nonventilated pediatric patients. Results: A 2‐month‐old infant developed cardiac tamponade secondary to tension pneumopericardium 11 days after cardiac surgery promptly resolved with pericardium drainage. We reviewed the literature on this topic and retrieved 50 cases, of which 72% were nontension whereas a minority were tension pneumopericardium (28%). Patients with tension pneumopericardium were mostly neonates (35.7% vs 22.2%), presented with an isolated air leak (64.3% vs 36.1%), and had a history of surgery (28.6% vs 8.3%) or hematological disease (28.6% vs 11.1%). In all nontension cases, treatment was conservative, whilst in all other cases, pericardiocentesis/pericardium drainage was carried out. There was a high survival rate (86.0%), which was lower in patients with tension pneumopericardium (71.4% vs 91.6%). Conclusions: Pneumopericardium is a rare condition with a higher mortality rate in patients with tension pneumopericardium, which requires immediate diagnosis and treatment. In nonventilated patients, tension pneumopericardium occurred more frequently in neonates, as an isolated air leak, and in those with a history of surgery or hematological disease.

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We report our clinical experience on the effect of Scrambler Therapy (ST) for a child with acute mixed pain refractory to pharmacological treatment. ST, recently proposed as an alternative treatment for chronic neuropathic pain in adults, is a noninvasive approach to relieve pain, by changing pain perception at brain level. It is safe and has no side effects. Further research is needed to assess its efficacy for acute pain and for paediatric population.

Fusarium species are ubiquitous pathogens causing opportunistic infections in immunocompromised patients. Clinical presentation depends on a host’s immunity and can be localized or disseminated. Since there are few reports of disseminated fusariosis in children, we described an unusual case of Fusarium solani infection in a 9-year-old child with acute lymphoblastic leukemia (ALL). This patient presented a deep wound in the elbow at diagnosis. During the induction phase of chemotherapy, he developed multiple skin lesions and severe pneumonia; Fusarium solani was cultured from the skin lesions. He was treated with a high dose of liposomal amphotericin B, followed by voriconazole. Starting from this peculiar case, we collected all patients with acute leukemia affected by Fusarium infection, treated in the pediatric Onco-Hematology Division of Padua University Hospital during the last 20 years. We identified another six cases: all these patients were affected by acute myeloid leukemia (AML) and five of them presented a relapsed/refractory disease. Two out of seven patients died because of infection; five patients recovered from infection, but three out of seven died because of leukemia. Skin lesions in immunocompromised patients should rise the suspicion of disseminated fusariosis. Furthermore, considering the emergence of filamentous fungi in immunocompromised patients, we all should be aware of Fusarium infection, reminding us that the diagnosis is important to cure the infection.

IntroductionPersisting and disabling depressive symptomatology represent a prominent feature of the post-acute COVID-19 syndrome. Sars-CoV-2-induced immune system dysregulation mainly result in a cytokine storm. Once in the brain, inflammatory mediators negatively affect neurotransmission, microglia activation, and oxidative stress, possibly disrupting critical brain neurocircuits which underpin depressive symptoms. So far, only inflammatory markers based on leukocyte counts have been linked to depressive outcome in COVID survivors. However, an accurate immune profile of post-COVID depression has yet to be elucidated.ObjectivesIdentify inflammatory mediators that predict post-COVID depression among a panel of cytokines, chemokines, and growth factors, with a machine learning routine.Methods88 COVID age- and sex-matched survivors’ (age 52.01 ± 9.32) were screened for depressive symptomatology one month after the virus clearance through the Beck Depression Inventory (BDI-13), with 12.5% of the individuals scoring in the clinical range (BDI-13 ≥ 9). Immune assay was performed through Luminex system on blood sampling obtained in the same context. We entered 42 analytes into an elastic net penalized regression model predicting presence of clinical depression, applied within a 5-fold nested cross-validation machine learning routine running in MATLAB. Significance of predictors was evaluated according to variable inclusion probability (VIP), as returned by 5000 bootstraps. Socio-demographics, previous psychiatric history, hospitalization, time after discharge were used as covariates.ResultsThe model reached a balance accuracy of 73% and AUC of 77%, correctly identifying 73% of people suffering from clinically relevant depressive symptoms (Figure1). Depressive symptomatology was predicted by high levels of CCL17, ICAM-1, MIF, whereas CXCL13, CXCL12, CXCL10, CXCL5, CXCL2, CCL23, CCL15, CCL8, GM-CSF showed a protective effect (Figure2).Image:Image 2:ConclusionsThis is the first study highlighting a putative inflammatory signature of post-COVID depression. Consistently to the immune profile of Major Depressive disorder, upregulation of innate immunity mediators seems to foster depressive symptoms in the aftermath of COVID. Interestingly, recruiters of B and T cells promoting a physiological adaptive response to viral infection also mitigate its psychiatric sequelae. Understanding the biological basis of post-COVID depression could pave the way for personalized treatments capable of reducing its add-on burden.Disclosure of InterestNone Declared