Corrigendum: Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

[This corrects the article DOI: 10.3389/fimmu.2023.1230049.].

Iatrogenic air embolism: pathoanatomy, thromboinflammation, endotheliopathy, and therapies.

Iatrogenic vascular air embolism is a relatively infrequent event but is associated with significant morbidity and mortality. These emboli can arise in many clinical settings such as neurosurgery, cardiac surgery, and liver transplantation, but more recently, endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and central and peripheral venous access and removal have overtaken surgery and trauma as significant causes of vascular air embolism. The true incidence may be greater since many of these air emboli are asymptomatic and frequently go undiagnosed or unreported. Due to the rarity of vascular air embolism and because of the many manifestations, diagnoses can be difficult and require immediate therapeutic intervention. An iatrogenic air embolism can result in both venous and arterial emboli whose anatomic locations dictate the clinical course. Most clinically significant iatrogenic air emboli are caused by arterial obstruction of small vessels because the pulmonary gas exchange filters the more frequent, smaller volume bubbles that gain access to the venous circulation. However, there is a subset of patients with venous air emboli caused by larger volumes of air who present with more protean manifestations. There have been significant gains in the understanding of the interactions of fluid dynamics, hemostasis, and inflammation caused by air emboli due to in vitro and in vivo studies on flow dynamics of bubbles in small vessels. Intensive research regarding the thromboinflammatory changes at the level of the endothelium has been described recently. The obstruction of vessels by air emboli causes immediate pathoanatomic and immunologic and thromboinflammatory responses at the level of the endothelium. In this review, we describe those immunologic and thromboinflammatory responses at the level of the endothelium as well as evaluate traditional and novel forms of therapy for this rare and often unrecognized clinical condition.

Extracorporeal membrane oxygenation in the management of granulomatosis with polyangiitis.

Granulomatosis with polyangiitis (GPA, also known as Wegener's granulomatosis) is a type of systematic vasculitis that primarily involves the lung and kidney. Diffuse alveolar hemorrhage (DAH) and associated acute respiratory failure are uncommon but devastating complications of GPA. Experience in using extracorporeal membrane oxygenation (ECMO) to manage DAH caused by GPA is limited. We report two GPA patients with DAH that were successfully managed using ECMO support. Examining 13 cases identified in the literature and two of our own, we observed that most patients experienced rapid deterioration in respiratory function in conjunction with a precedent respiratory infection. All 15 patients received veno-venous ECMO support. The median duration of ECMO support was 11 days (interquartile range: 7.5-20.75 days). Bleeding was the most common complication, seen in four (26.7%) cases. All patients were successfully weaned off ECMO after a median length of hospital stay of 42 days (interquartile range: 30-78 days). We demonstrated that the use of ECMO is a reasonable and effective support option in the management of GPA patients with DAH. The risk of bleeding is high but maybe reduced using a lower anticoagulation goal.

Prolonged use of eptifibatide as a bridge to maintain drug-eluting stent patency in a patient receiving extracorporeal membrane oxygenation.

BACKGROUND: Venoarterial extracorporeal membrane oxygenation (VA-ECMO) has been used as a bridge to cardiac recovery in patients following a major cardiac event. There is a lack of literature surrounding prolonged use of eptifibatide and optimal dosing during ECMO. This case report describes our experience with extended durations and standard dosing of eptifibatide in the setting of ECMO. CASE: A 40-year-old male with a history of Marfan's syndrome, aortic root and ascending aortic aneurysm status post a modified Bentall with a St. Jude mechanical aortic valve conduit and hemi-Cabrol with a Dacron graft to the left main coronary artery presented with exertional chest pain and was found to have an anastomotic narrowing to the left main which occluded while awaiting surgical revision. A rescue percutaneous coronary intervention at the anastomotic site was performed. Due to hemodynamic instability, he was placed on femoral VA-ECMO. The patient was started on anticoagulation for the ECMO circuit and eptifibatide to maintain stent patency. The patient experienced several bleeding episodes for which he received supportive care, endoscopic intervention and left gastric artery embolization. Eptifibatide was maintained at standard dosing and the heparin infusion was withheld. A coronary angiogram revealed no thrombus within the Cabrol graft a patent stent previously placed at the site of the distal graft-coronary anastomosis. The patient was decannulated from ECMO and underwent coronary artery bypass grafting and division of the hemi-Cabrol graft. CONCLUSION: While eptifibatide was effective in maintaining stent patency, our patient experienced several bleeding episodes during ECMO. Thus, the risks and benefits of concurrent antiplatelet and anticoagulant therapy must be appropriately weighed in this patient population. Additionally, as the need for dual antiplatelet therapy due to coronary stent implantation is increasing, further studies are needed to validate optimal dosing of eptifibatide in patients at a high risk of bleeding during ECMO.

Hemolysis following wrap aortoplasty for Type A aortic dissection repair: Case report and review of the literature.

A Dacron wrap aortoplasty has been described as an adjunct to reduction ascending aortoplasty for the repair of Type A aortic dissections. We report a case of an uncomplicated hemiarch repair with wrap aortoplasty of the distal anastomosis which resulted in severe acute hemolysis. Despite only minimal focal graft deformation on imaging, the patient was found to have a flow gradient across the distal anastomosis, which was reduced by > 50% following release of the outer graft wrap. To our knowledge, only 29 additional cases of hemolytic anemia following aortic dissection repair have been described in the English literature. The reported mechanisms included aortic graft stenosis (50%), graft kinking (23%), external compression of the graft (20%), and a folded elephant trunk appendage (7%). The mean onset of hemolysis following aortic dissection repair occurred 32.2 ± 44.4 months after surgery, with only 16.7% of cases occurring within 2 weeks. This review details the clinical, laboratory, and imaging findings suggestive of mechanical hemolysis following aortic surgery.

Delayed Retrograde Ascending Aortic Dissection After Endovascular Repair of Descending Dissection.

We report the case of a 34-year-old woman who developed delayed retrograde ascending aortic dissection after previous endovascular repair of her descending thoracic aorta. Preoperative computed tomography imaging specifically highlights the interaction of endograft springs with the dissection flap and surrounding aortic tissues. Intraoperative findings are presented for comparison and further discussion.

Repair of a complex thoracic aneurysm from relapsing polychondritis.

A 29-year-old female with a history of relapsing polychondritis (RP) and open repair of a proximal descending thoracic aneurysm presented with 2 areas of asymptomatic thoracic aortic aneurysmal dilatation. The patient returned 3 months later with symptomatic aneurysm expansion, and she underwent ascending aortic arch replacement. She subsequently underwent staged endovascular repair of the distal descending thoracic aorta. RP is a rare disorder with an incidence of 3.5 per million persons annually, 4% to 7% of whom develop aneurysmal disease. Because of the aneurysmal potential of this disease, it is important for vascular surgeons to be aware of its presentation and treatment. To our knowledge, this is the first reported case describing endovascular technique to treat such a patient.

Perioperative management of patients undergoing transmyocardial laser revascularization.

Advanced revascularization strategies continue to uncover a growing number of patients with symptomatic diffuse coronary artery disease. Transmyocardial laser revascularization (TMR) provides significant benefit in terms of improved quality of life and more complete revascularization for these difficult to treat patients when TMR is used as sole therapy or in combination with coronary artery bypass grafting. The safe clinical application of this important procedure relies on diligent perioperative management with appropriate patient selection, intraoperative care that avoids myocardial ischemia, and postoperative pain control along with expeditious reinstitution of antianginal medications. The treatment paradigms learned with the safe application of TMR should prove useful as new therapies to extend our revascularization options are developed.

Transmyocardial laser revascularization as an adjunct to coronary artery bypass grafting: a randomized, multicenter study with 4-year follow-up.

We evaluated transmyocardial laser revascularization (TMLR) with coronary artery bypass grafting (CABG) versus CABG alone for severe coronary artery disease involving 21 myocardial region unsuited for CABG. At 4 centers, 44 consecutive patients were randomized for CABG+TMLR (n = 23) or CABG alone (n = 21). Operative and in-hospital mortality and morbidity rates were monitored. Clinical status was evaluated at hospital discharge, 1 year, and 4 years. Success was characterized by relief of angina and freedom from repeat revascularization and death. Preoperatively, 20 patients (47%) were at high risk. The CABG technique, number of grafts, and target vessels were similar in both groups. Patients undergoing CABG+TMLR received 25 +/- 11 laser channels. Their < or = 30-day mortality was 13% (3/23) compared with 28% (6/21) after CABG alone (P = 0.21). There were no significant intergroup differences in the number of intraoperative or in-hospital adverse events. The follow-up period was 50.3 +/- 17.8 months for CABG alone and 48.1 +/- 16.8 months for CABG+TMLR. Both groups had substantially improved angina and functional status at 1 and 4 years, with no significant differences in cumulative 4-year mortality. The incidence of repeat revascularization was 24% after CABG alone versus none after CABG+TMLR (P < 0.05). The 4-year event-free survival rate was 14% versus 39%, respectively (P < 0.064). In conclusion, CABG+TMLR appears safe and poses no additional threat for high-risk patients. Improved overall success and repeat revascularization rates may be due to better perfusion of ischemic areas not amenable to bypass. Further studies are warranted to determine whether these trends are indeed significant.