We conducted a cross-sectional study to identify the demographic predictors of traumatic brain injury (TBI), and the risk of association of psychiatric comorbidities including alcohol use disorder (AUD) and TBI-related hospitalizations in the children and adolescent population. Methods We included 3,825,523 children and adolescent inpatients (age 8-18 years) using the nationwide inpatient sample (NIS) database (2010-2014), and 61,948 inpatients had a primary diagnosis of TBI. These inpatients were grouped by comorbid AUD (N = 2,644). Multivariable logistic regression model adjusted for demographics, and psychiatric comorbidities including other substance use disorders (SUDs) was used to evaluate the odds ratio (OR) of AUD as a risk factor for TBI-related hospitalization. Results The majority of the TBI inpatients were adolescents (12-18 years, 82.2%), males (71.2%), and whites (59.2%). Males had three times higher odds (95% CI 3.14-3.26) for TBI-related hospitalization compared to females. Among psychiatric comorbidities, mood (4.1%) and anxiety (2.2%) disorders were prevalent in TBI inpatients, and were not associated with increased odds for TBI-related hospitalization. Among SUD, alcohol and tobacco use (4.4% each), and cannabis use (3.5%) were prevalent, and among all substances, AUD was associated with higher odds (OR 3.5, 95% CI 3.35-3.67) of TBI-related hospitalization. These patients with TBI and comorbid AUD also had higher odds for abusing stimulants (OR 5.11, 95% CI 3.85-6.77), cannabis (OR 4.69, 95% CI 4.12-5.34), and tobacco (OR 3.77, 95% CI 3.34-4.27). Conclusion AUD is an independent risk factor for TBI-related hospitalization with an increased risk of 50% in the children and adolescent population compared to non-alcohol users. TBI inpatients with AUD are prevalent in white, and male adolescents. These at-risk populations are also at higher risk of comorbid mood disorders and increased substance use including stimulants, cannabis, and tobacco.

We aimed to analyze the differences in demographics, comorbidities, and the risk of in-hospital mortality in pediatric arterial ischemic stroke (PAIS) inpatient population by hematological (HEM) and cardiovascular (CV) risk factors. Methods A total of 4,036 inpatients (1-18 years of age) from the Nationwide Inpatient Sample (NIS) with a primary diagnosis of PAIS were included. Descriptive statistics, linear-by-linear association test, and logistic regression models were utilized to analyze differences in demographics, comorbidities, and their impact on mortality in PAIS inpatients by CV and HEM risk factors. Results The cumulative in-hospital mortality rate in the entire PAIS inpatient cohort was 3.6%. The mortality rate was higher in the CV cohort (57.4%) as compared to the HEM cohort (29.7%). When compared with the cohort with no risk factors, HEM and CV were associated with four times (95% CI: 2.36-8.03) and seven (95% CI: 4.03-12.61) times higher odds for in-hospital mortality respectively. CV risk factors like cardiomyopathy and diabetes, and HEM risk factors like blood disorders, coagulation disorders, and deficiency anemias were associated with a significantly increased risk of in-hospital mortality. Conclusion The in-hospital mortality risk in PAIS patients was increased by 613% by CV risk factors and by 336% by HEM risk factors. Early identification and effective management of associated CV and HEM risk factors in the PAIS patient population can pave the way for increased survival and improved clinical outcomes.

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Figure 1. Haematoxylin and eosin stain showing poorly differentiated polygonal cells containing eccentrically located nuclei and abundant eosinophilic cytoplasm with cells arranged in solid nests. 2. Hep-par stain positivity suggestive of hepatocellular carcinoma. 3. Cytokeratin-7 stain diffusely positive favoring lung as the primary tumor site.

The COVID-19 virus has impacted global health on a wide scale, affecting humans of all ages and ethnicities. While most have mild upper respiratory viral symptoms, some have died due to severe pneumonia, acute respiratory distress syndrome (ARDS), or coagulopathies to mention a few. It has been postulated that the COVID-19 virus can initiate an autoinflammatory reaction in the body via multiple pathways of cytokine activation. The virus can cause delayed response after 4–8 weeks of acute infection, which resembles a cytokine storm or MAS (macrophage activation syndrome). This highly inflammatory syndrome, called MIS-C or multisystem inflammatory response syndrome, needs to be diagnosed and treated early to prevent multiorgan damage and mortality. There are widespread lab abnormalities including highly elevated acute phase reactants ferritin, D-Dimer, lactate dehydrogenase (LDH), creatinine kinase (CK), sedimentation rate (ESR), and C-reactive protein (CRP) as well as markers of cardiac damage including troponin and brain natriuretic peptide (BNP). The syndrome can present in unique ways from classic MIS-C with hypovolemic shock to Kawasaki disease-like presentation. We present a case of a 12-year-old boy who presented to Le Bonheur Children’s Hospital in Memphis with classic signs and symptoms of “severe” MIS-C requiring intubation, multiple pressors, ECMO, and renal replacement therapy. He was treated successfully with immunomodulating medicines including intravenous immune globulin (IVIG), steroids, interleukin-6 inhibitor, tumor necrosis factor-a inhibitor, interleukin-1 inhibitor, and Janus kinase inhibitor.