Open chest and pericardium facilitate transpulmonary passage of venous air emboli

Storm, Benjamin; Halvorsen, Per Steinar; Skulstad, Helge; Dybwik, Knut; Schjalm, Camilla; Christiansen, Dorte; Wisløff-Aase, Kristin; Fosse, Erik; Braaten, Tonje; Mollnes, Tom Eirik

doi:10.1111/aas.13796

Cited by 7 publications

(20 citation statements)

References 13 publications

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“…If our ex vivo findings translate to in vivo conditions, we suggest that clinicians should maintain a strong focus on the detection of air emboli, such as by using echocardiography as described in a pig model ( 49 ), during high-risk procedures such as thoracic surgery, hysteroscopy, or extracorporeal blood circulation. Our findings suggest that C3 inhibition might dampen the thromboinflammatory response and could be a future approach for treatment.…”

Section: Discussionmentioning

confidence: 99%

Air Bubbles Activate Complement and Trigger Hemostasis and C3-Dependent Cytokine Release Ex Vivo in Human Whole Blood

Storm

Christiansen

Fure

et al. 2021

The Journal of Immunology

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Venous air embolism, which may complicate medical and surgical procedures, activates complement and triggers thromboinflammation. In lepirudin-anticoagulated human whole blood, we examined the effect of air bubbles on complement and its role in thromboinflammation. Whole blood from 16 donors was incubated with air bubbles without or with inhibitors of C3, C5, C5aR1, or CD14. Complement activation, hemostasis, and cytokine release were measured using ELISA and quantitative PCR. Compared with no air, incubating blood with air bubbles increased, on average, C3a 6.5-fold, C3bc 6-fold, C3bBbP 3.7-fold, C5a 4.6-fold, terminal complement complex sC5b9 3.6-fold, prothrombin fragments 1+2 (PTF1+2) 25-fold, tissue factor mRNA (TF-mRNA) 26-fold, microparticle tissue factor 6.1-fold, β-thromboglobulin 26-fold (all p < 0.05), and 25 cytokines 11-fold (range, 1.5–78-fold; all p < 0.0001). C3 inhibition attenuated complement and reduced PTF1+2 2-fold, TF-mRNA 5.4-fold, microparticle tissue factor 2-fold, and the 25 cytokines 2.7-fold (range, 1.4–4.9-fold; all p < 0.05). C5 inhibition reduced PTF1+2 2-fold and TF-mRNA 12-fold (all p < 0.05). C5 or CD14 inhibition alone reduced three cytokines, including IL-1β (p = 0.02 and p = 0.03). Combined C3 and CD14 inhibition reduced all cytokines 3.9-fold (range, 1.3–9.5-fold; p < 0.003) and was most pronounced for IL-1β (3.2- versus 6.4-fold), IL-6 (2.5- versus 9.3-fold), IL-8 (4.9- versus 8.6-fold), and IFN-γ (5- versus 9.5-fold). Antifoam activated complement and was avoided. PTF1+2 was generated in whole blood but not in plasma. In summary, air bubbles activated complement and triggered a C3-driven thromboinflammation. C3 inhibition reduced all mediators, whereas C5 inhibition reduced only TF-mRNA. Combined C5 and CD14 inhibition reduced IL-1β release. These data have implications for future mechanistic studies and possible pharmacological interventions in patients with air embolism.

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Section: Discussionmentioning

confidence: 99%

Air Bubbles Activate Complement and Trigger Hemostasis and C3-Dependent Cytokine Release Ex Vivo in Human Whole Blood

Storm

Christiansen

Fure

et al. 2021

The Journal of Immunology

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“…We used continuous M-mode and intermittent 2D transesophageal echocardiography (TEE) to verify intraosseous infusion and to detect the systemic passage of emboli by obtaining an echocardiographic window of both the pulmonary artery and the left ventricular outlet tract (LVOT) as described by Storm et al [22]. We registered elapsed time and eventual systemic passage of emboli.…”

Section: Exsanguination Intraosseous Infusion and Data Collectionmentioning

confidence: 99%

“…We expected to nd systemic fat emboli in 80% of the animals with an open chest, and 10% of the animals with a closed chest, based on previous experience with similar animal models using intravenously injected air [22]. An online sample calculator (https://clincalc.com/stats/samplesize.aspx) with a 2:1 enrolment ratio, alpha of 5%, and power of 80%, yielded a group-size of 14 with 7 pigs in each group allocated to either open or closed chest.…”

Section: Power Calculationmentioning

confidence: 99%

“…We believed that an open chest would cause reduced transmural lung pressure, allowing over-expansion of the lungs. This, in conjunction with mechanical ventilation, has been proposed to facilitate the recruitment of extra-alveolar shunt vessels, thus opening up dynamic passages available for systemic shunting for air emboli [22,40]. Fat emboli likely do not share the gravitational, thrombogenic, or physical properties of air emboli, and are probably in uenced by the mentioned factors in other ways.…”

Section: Systemic Embolizationmentioning

confidence: 99%

“…It has been proposed that open chest, e.g. after emergency thoracotomy [21], may increase the occurrence of systemic air embolization [22]. We, therefore, hypothesized that intraosseous uid resuscitation would generate both pulmonary and systemic fat emboli, and that open chest would increase systemic embolization.…”

Section: Introductionmentioning

confidence: 95%

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Intraosseous Fluid Resuscitation Causes Systemic Fat Emboli in a Porcine Hemorrhagic Shock Model

Kristiansen

Storm

Dahle

et al. 2021

Preprint

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BackgroundIntraosseous cannulation can be life-saving when intravenous access cannot be readily achieved. However, it has been shown that the procedure may cause fat emboli to the lungs and brain. Fat embolization may cause serious respiratory failure and fat embolism syndrome. We investigated whether intraosseous fluid resuscitation in pigs in hemorrhagic shock caused pulmonary or systemic embolization to the heart, brain, or kidneys and if this was enhanced by open chest conditions.MethodsWe induced hemorrhagic shock in anesthetized pigs followed by fluid-resuscitation through bilaterally placed tibial intraosseous cannulas. A subgroup underwent median sternotomy with pericardiectomy and pleurotomy before hemorrhagic shock was induced. We used invasive hemodynamic and respiratory monitoring including Swan Ganz pulmonary artery catheter and transesophageal echocardiography and obtained biopsies from the lungs, heart, brain, and left kidney postmortem.ResultsAll pigs exposed to intraosseous infusion had pulmonary fat emboli in postmortem biopsies. Additionally, seven of twenty-one pigs had coronary fat emboli. None of the pigs with open chest had fat emboli in postmortem lung, heart, or kidney biopsies. During fluid-resuscitation, three pigs developed significant ST-elevations on ECG; all of these animals had coronary fat emboli on postmortem biopsies. ConclusionsSystemic fat embolism occurred in the form of coronary fat emboli in a third of the animals who underwent intraosseous fluid resuscitation. Open chest conditions did not increase the incidence of systemic fat embolization.

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Hands-free continuous carotid Doppler ultrasound for detection of the pulse during cardiac arrest in a porcine model

et al. 2023

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Open chest and pericardium facilitate transpulmonary passage of venous air emboli

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 7 publications

References 13 publications

Air Bubbles Activate Complement and Trigger Hemostasis and C3-Dependent Cytokine Release Ex Vivo in Human Whole Blood

Air Bubbles Activate Complement and Trigger Hemostasis and C3-Dependent Cytokine Release Ex Vivo in Human Whole Blood

Intraosseous Fluid Resuscitation Causes Systemic Fat Emboli in a Porcine Hemorrhagic Shock Model

Hands-free continuous carotid Doppler ultrasound for detection of the pulse during cardiac arrest in a porcine model

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