Comparison of septic and nonseptic pulmonary embolism in children

Abstract

Background Septic pulmonary embolism (SPE) in children is a rare disease. Data are scarce regarding the clinical and laboratory manifestation of SPE compared with nonseptic pulmonary embolism (ns‐PE). Furthermore, specific guidelines for the management of SPE in children are lacking. Aim We compared the clinical course and outcome of children with SPE and ns‐PE. Methods A retrospective, cohort study of hospitalized children, 2005–2020, with documented pulmonary embolism imaging. Results Sixteen children (eight SPE, eight ns‐PE) were identified. Episodes of SPE occurred secondary to endocarditis, musculoskeletal and soft tissue infections, with Staphylococcus aureus (n = 4) and streptococcus spp. (n = 2) as the most common pathogens. Radiographically, SPE presented as a microvascular disease with parenchymatic nodules/cavitations, whereas ns‐PE presented as larger vessel disease with filling defects. Risk factors (including thrombophilia) were noted in 0% and 87.5% of SPE and ns‐PE patients, respectively (p < .01). Pulmonary embolism diagnosis was delayed in SPE compared with ns‐PE (median: 8.5 days vs. 1 day). The SPE group had higher rates of fever (100% vs. 12.5%, p < .01), C‐reactive protein (CRP levels; 18.49 vs. 4.37 mg/dl, p = .02), and fibrinogen levels (880 vs. 467 mg/dl, p < .001). Antithrombotic treatment for >4 months was administrated to 14.3% and 87.5% of SPE and ns‐PE patients, respectively (p < .01). One ns‐PE patient had a second thromboembolic event compared to none in the SPE group. Conclusions SPE in children is a unique subgroup of PE with different clinical and laboratory findings that requires a different diagnostic approach and probably shorter duration of antithrombotic treatment.

The Neglected Fact

“…In children, the diagnosis of PE may be missed or delayed, mainly because of the rarity of the disease. It is noteworthy that in the previous literature, the lag between clinical manifestations and diagnosis was shown to be approximately 0 to 42 days, while in another study in children, the lag time was 1 to 16 days 1,2 . Computed tomography pulmonary angiography is the preferred diagnostic modality, while ventilation perfusion scans and routine pulmonary angiography are used less frequently 10,15 .…”

“…It is noteworthy that in the previous literature, the lag between clinical manifestations and diagnosis was shown to be approximately 0 to 42 days, while in another study in children, the lag time was 1 to 16 days. 1,2 Computed tomography pulmonary angiography is the preferred diagnostic modality, while ventilation perfusion scans and routine pulmonary angiography are used less frequently. 10,15 Ddimer levels are significantly elevated in approximately 80% of PE children, and electrocardiogram (ECG) shows changes in sinus tachycardia, T-wave inversion, and right bundle branch block.…”

“…In a small number of cases, particularly in patients with right ventricular dysfunction and/or hemodynamic instability, the use of tissue plasminogen activator thrombolysis, thrombosis, or extracorporeal membrane oxygenation support is first considered. 1,2 In a cohort study in Canada, 35% of children with large or sublarge area PE had adverse outcomes with 13% of children with nonlarge area PE, more specifically the progression or recurrence of PE, chronic thromboembolic pulmonary hypertension, and major bleeding associated with thrombolysis or PE. 10 In existing cohort studies, the high risk of death in patients with large areas of PE has been demonstrated.…”

“…Previous literature has described the efficacy and safety of low molecular weight heparin in children with nonseptic PE for 2 to 12 months. In a small number of cases, particularly in patients with right ventricular dysfunction and/or hemodynamic instability, the use of tissue plasminogen activator thrombolysis, thrombosis, or extracorporeal membrane oxygenation support is first considered 1,2 …”

“…Depending on the severity of the clinical presentation, pulmonary embolism is classified as (1) high risk (significant impairment of the cardiovascular system with significant hemodynamic changes), (2) moderate risk (right ventricular injury and/ or elevated troponin I or B type natriuretic peptide, no systemic hemodynamic changes), and (3) low risk. [1][2][3] In pulmonary embolism caused by septic infection, embolism originates from infectious microcirculation lesions such as endovascular catheterization, endocarditis, osteomyelitis and septic arthritis, liver and kidney abscesses, skin and soft tissue infections, and periodontal abscesses. 4 Pulmonary embolism is considered a rare disease in children and is often overlooked.…”