PB0654 - Hospital-acquired venous thromboembolism among critically ill children undergoing invasive ventilation for acute respiratory failure is associated with impaired clot formation and fibrinolysis

Monday, June 24, 2024

13:45 – 14:45 ICT

Room: Exhibition Hall

Presenting Author(s)

Steven Bruzek, MS

Program Manager - Clinical and Translational Research
Johns Hopkins All Children's Hospital
Saint Petersburg, Florida, United States

Co-Author(s)

Vera Ignjatovic, PhD, MBA

Professor of Pediatrics
Johns Hopkins All Children's Institute for Clinical and Translational Research; Department of Pediatrics, School of Medicine, Johns Hopkins University, United States
St Petersburg, Florida, United States
Neil Goldenberg, MD,PhD

Departments of Pediatrics and Medicine
Johns Hopkins University School of Medicine, Baltimore, MD; Clinical and Data Coordinating Center for Pediatric Multicenter Studies, Johns Hopkins All Children’s Institute for Clinical and Translational Research, St. Petersburg, FL
Saint Petersburg, Florida, United States
AS

Anthony Sochet

Assistant Professor
Department of Anesthesiology and Critical Care Medicine, School of Medicine, Johns Hopkins University
Saint Petersburg, Florida, United States

Background: Critically ill children requiring invasive mechanical ventilation (IMV) have an increased risk of hospital-acquired venous thromboembolism (HA-VTE) with rates between 4.4-16.5%. No study has characterized plasma coagulative and fibrinolytic dysfunction in this population.

Aims: To characterize plasma coagulative and fibrinolytic function using the modified mini-Euglobulin Clot Lysis Assay (mmECLA) and Clot Formation and Lysis (CloFAL) assays. We hypothesized that children undergoing IMV who developed a HA-VTE, compared to those who did not, would exhibit impaired functional fibrinolysis and hypercoagulability.

Methods: We performed a single center, observational cohort study including children < 18 years of age who underwent acute IMV. After IRB approval and informed consent, samples were collected at 24- and 48-hours following endotracheal intubation in sodium citrate tubes, with resulting platelet-poor plasma analyzed. Primary outcomes were assay indices and their slopes of change between sampling times compared by cohorts defined by presence of HA-VTE with a subgroup analysis by age groupings: 0-1 and 10-18 years.

Results: Of the 58 patients studied, HA-VTE incidence was 12.1%. There were no differences for those with and without HA-VTE for age, gender, IMV duration, mortality, presence/absence of viral infection or bacterial pneumonia, oxygenation index, or assay indices at independent collection times (Table 1). However, differences in paired analyses were noted between sampling time points, including an increased clotting capacity (CloFAL Clotting Index [CI%]; mmECLA Delta OD Ratio [DODR]) comparing those with and without HA-VTE (Figure 1). Patients with HA-VTE aged 0-1 years (n=3) and 10-18 years (n=4) had decreased functional fibrinolysis (decreased CloFAL fibrinolytic index [FI2%] and greater mmECLA Clot Lysis Time Ratios [CLTR]) from 24- to 48-hours, compared to age-matched children without HA-VTE (Figure 1).

Conclusion(s): Among critically ill children undergoing acute IMV for respiratory failure, those who developed HA-VTE exhibited impaired plasma fibrinolytic and coagulative function compared to children without HA-VTE.