Systematic review of risk factors and outcomes of post-implantation syndrome following endovascular aortic repair.

OBJECTIVE: Post implantation syndrome (PIS) is an early systemic inflammatory response following endovascular aortic repair (EVAR). The response is variable in patients and the clinical significance of PIS upon outcomes is unknown. This study aims to evaluate the incidence, risk factors, and prognostic implication of PIS. METHODS: Systematic literature review and analysis was performed in accordance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) and Cochrane guidelines of PubMed, Scopus, ClinicalTrials.gov, and the Cochrane Central Register of Controlled Trials. Eligible English-language studies regarding PIS after infrarenal EVAR were included, after removing duplicates. RESULTS: After screening, 31 studies were included. A total of 2847 patients were reviewed, with mean age of 70.7 years, of which 2012 (90.4%) were male, with a pooled mean follow-up of 26.1 months. PIS was reported in 25.3% of cases, with mean aneurysm diameter of 56.4 cm. Polytetrafluoroethylene (PTFE) grafts were utilized in 794 patients (27.9%) with polyester in 1839 (64.6%). White blood cell count, C-reactive protein, interleukin (IL)-6, IL-8, and IL-10 levels were all significantly elevated postoperatively. Thirty-day outcomes included type I endoleak rate of 0.8%, type II endoleak rate of 1.7%, reintervention rate of 0.35%, and mortality rate of 0.25%. Subgroup pooled analysis of patients with PIS (n = 309) vs No-PIS (n = 691) revealed that polyester (n = 642), rather than PTFE (n = 234) grafts, were associated with a higher rate of PIS (94.8% vs 3.7%; P = .0001), White blood cell count was higher in the PIS group both preoperatively (7.61 vs 6.76 × 109/L; P = .04) and postoperatively (15.0 vs 9.8 × 109/L; P = .0007) and IL-6 levels were higher in the PIS group postoperatively (98.6 vs 25.2 pg/mL; P = .02). Aneurysm diameter and amount of chronic or new thrombus within the aneurysm sac was not identified as a risk factor for PIS. Pooled outcomes of patients with PIS vs No-PIS demonstrated a significantly higher rate of 30-day mortality (0.6% vs 0%; P = .03) and major adverse cardiac events (5.8% vs 0.43%; P < .0001) without any differences seen in reintervention or 30-day type I or type II endoleaks. CONCLUSIONS: This systematic review suggests that polyester grafts are strongly associated with PIS compared with PTFE. Interestingly, this report is suggestive of an association between 30-day mortality and major adverse cardiac events and PIS. Given these clinical sequelae, consideration for use of PTFE over polyester grafts to reduce the incidence of PIS may be a simple step to improve overall outcome. Further, exploration of the relationship between inflammatory mediators associated with PIS and mortality and cardiac complications may engender deeper understanding of risks, leading to eventual mitigation of harm for patients experiencing PIS.

Secretory phospholipase A2 in SARS-CoV-2 infection and multisystem inflammatory syndrome in children (MIS-C).

Secretory phospholipase 2 (sPLA2) acts as a mediator between proximal and distal events of the inflammatory cascade. Its role in SARS-CoV-2 infection is unknown, but could contribute to COVID-19 inflammasome activation and cellular damage. We present the first report of plasma sPLA2 levels in adults and children with COVID-19 compared with controls. Currently asymptomatic adults with a history of recent COVID-19 infection (≥4 weeks before) identified by SARS-CoV-2 IgG antibodies had sPLA2 levels similar to those who were seronegative (9 ± 6 vs.17 ± 28 ng/mL, P = 0.26). In contrast, children hospitalized with severe COVID-19 had significantly elevated sPLA2 compared with those with mild or asymptomatic SARS-CoV-2 infection (269 ± 137 vs. 2 ± 3 ng/mL, P = 0.01). Among children hospitalized with multisystem inflammatory syndrome in children (MIS-C), all had severe disease requiring pediatric intensive care unit (PICU) admission. sPLA2 levels were significantly higher in those with acute illness <10 days versus convalescent disease ≥10 days (540 ± 510 vs. 2 ± 1, P = 0.04). Thus, sPLA2 levels correlated with COVID-19 severity and acute MIS-C in children, implicating a role in inflammasome activation and disease pathogenesis. sPLA2 may be a useful biomarker to stratify risk and guide patient management for children with acute COVID-19 and MIS-C. Therapeutic compounds targeting sPLA2 and inflammasome activation warrant consideration.

Prevalence of SARS-CoV-2 antibodies in pediatric healthcare workers.

OBJECTIVES: To determine SARS-CoV-2-antibody prevalence in pediatric healthcare workers (pHCWs). DESIGN: Baseline prevalence of anti-SARS-CoV-2-IgG was assessed in a prospective cohort study from a large pediatric healthcare facility. Prior SARS-CoV-2 testing history, potential risk factors and anxiety level about COVID-19 were determined. Prevalence difference between emergency department (ED)-based and non-ED-pHCWs was modeled controlling for those covariates. Chi-square test-for-trend was used to examine prevalence by month of enrollment. RESULTS: Most of 642 pHCWs enrolled were 31-40years, female and had no comorbidities. Half had children in their home, 49% had traveled, 42% reported an illness since January, 31% had a known COVID-19 exposure, and 8% had SARS-CoV-2 PCR testing. High COVID-19 pandemic anxiety was reported by 71%. Anti-SARS-CoV-2-IgG prevalence was 4.1%; 8.4% among ED versus 2.0% among non-ED pHCWs (p < 0.001). ED-work location and known COVID-19 exposure were independent risk factors. 31% of antibody-positive pHCWs reported no symptoms. Prevalence significantly (p < 0.001) increased from 3.0% in April-June to 12.7% in July-August. CONCLUSIONS: Anti-SARS-CoV-2-IgG prevalence was low in pHCWs but increased rapidly over time. Both working in the ED and exposure to a COVID-19-positive contact were associated with antibody-seropositivity. Ongoing universal PPE utilization is essential. These data may guide vaccination policies to protect front-line workers.

Utility of Point-of-Care Lung Ultrasonography for Evaluating Acute Chest Syndrome in Young Patients With Sickle Cell Disease.

STUDY OBJECTIVE: Acute chest syndrome is a leading cause of mortality in patients with sickle cell disease (SCD). Because early detection of acute chest syndrome is directly tied to prognosis, young patients with SCD undergo countless chest radiography screenings throughout their lifetime for commonly occurring acute chest syndrome risk factors such as fever, chest pain, or cough. Chest radiography is not an ideal screening method because it is associated with radiation exposure, which accumulates with repeated imaging. Point-of-care lung ultrasonography is a nonradiating imaging modality that has been used to identify other lung pathology and may have a role in SCD. The goal of this study was to determine the accuracy of point-of-care lung ultrasound to identify an infiltrate suggestive of acute chest syndrome in patients with SCD compared to chest radiography as the gold standard. METHODS: This was a prospective observational study in 2 urban pediatric emergency departments to evaluate the accuracy of point-of-care lung ultrasonography in identifying patients with SCD who were aged 0 to 21 years and had an infiltrate suggestive of acute chest syndrome compared with chest radiography. Clinicians and trainees with point-of-care lung ultrasonographic training obtained informed consent and performed investigational point-of-care lung ultrasonography to evaluate for lung consolidation. A blinded point-of-care lung ultrasonographic expert reviewed results for quality assurance and agreement. Accuracy, sensitivity, specificity, likelihood ratios, and positive and negative predictive value were calculated for point-of-care lung ultrasonography test performance characteristics, with chest radiography as a reference standard. RESULTS: Point-of-care lung ultrasonography was performed on 191 SCD patients with a mean age of 8 years; 41% were female patients, and there was a 17% prevalence of acute chest syndrome. Accuracy of point-of-care lung ultrasonography to detected acute chest syndrome was 92%, sensitivity was 88%, and specificity was 93% compared with that for chest radiography. CONCLUSION: Point-of-care lung ultrasonography is a feasible alternative to chest radiography for screening for acute chest syndrome in young patients with SCD. Further studies are needed to determine how this test performs within clinical practice.

Impact of arginine therapy on mitochondrial function in children with sickle cell disease during vaso-occlusive pain.

Altered mitochondrial function occurs in sickle cell disease (SCD), due in part to low nitric oxide (NO) bioavailability. Arginine, the substrate for NO production, becomes acutely deficient in SCD patients with vaso-occlusive pain episodes (VOE). To determine if arginine improves mitochondrial function, 12 children with SCD-VOE (13.6 ± 3 years; 67% male; 75% hemoglobin-SS) were randomized to 1 of 3 arginine doses: (1) 100 mg/kg IV 3 times/day (TID); (2) loading dose (200 mg/kg) then 100 mg/kg TID; or (3) loading dose (200 mg/kg) followed by continuous infusion (300 mg/kg per day) until discharge. Platelet-rich plasma mitochondrial activity, protein expression, and protein-carbonyls were measured from emergency department (ED) presentation vs discharge. All VOE subjects at ED presentation had significantly decreased complex-V activity compared to a steady-state cohort. Notably, complex-V activity was increased at discharge in subjects from all 3 arginine-dosing schemes; greatest increase occurred with a loading dose (P < .001). Although complex-IV and citrate synthase activities were similar in VOE platelets vs steady state, enzyme activities were significantly increased in VOE subjects after arginine-loading dose treatment. Arginine also decreased protein-carbonyl levels across all treatment doses (P < .01), suggesting a decrease in oxidative stress. Arginine therapy increases mitochondrial activity and reduces oxidative stress in children with SCD/VOE. This trial was registered at www.clinicaltrials.gov as #NCT02536170.