Does the aerosol box accommodate the double-lumen tube intubation?

The aerosol box was widely used to shield healthcare providers from exposure to COVID-19 during single-lumen intubation procedures. However, it has not previously been evaluated for its use in double-lumen tube intubations. This report presents the case of a 25-year-old COVID-19-positive male with a fever who required an emergency thoracotomy for a mediastinal abscess. During the rapid-sequence induction of general anesthesia, an attempt to use the aerosol box for double-lumen tube intubation was made. The attempt faced unique challenges due to the aerosol box's restrictive dimensions and the double-lumen tube's physical characteristics, such as length and flexibility, resulting in an unsuccessful first attempt. Consequently, the aerosol box was removed, and a successful intubation was achieved without it. Postoperatively, the patient remained intubated, was transferred to the intensive care unit, and was extubated on the second postoperative day, followed by intensive care unit discharge. This experience suggests that the standard aerosol box size (50 cm wide, 40 cm deep, and 50 cm tall) may not be suitable for double-lumen tube intubations. This highlights the importance of assessing the feasibility of each aerosol box before its clinical use in such procedures.

Emergent veno-venous extracorporeal membrane oxygenation during aortic valve replacement following severe re-expansion pulmonary edema: A case report.

Re-expansion pulmonary edema is defined as pulmonary edema that occurs when a chronically collapsed lung rapidly re-expands, most commonly following chest tube placement for pneumothorax, re-expansion of severe atelectasis, and evacuation of pleural effusion. Though it is very rare, the sudden onset and clinical features of re-expansion pulmonary edema make it a lethal complication that requires urgent treatment. We present a 60-year-old patient who underwent an aortic valve replacement with pre-existing large bilateral pleural effusions. Intraoperatively, upon evacuation of the pleural effusions, the patient developed worsening lung compliance, refractory hypoxemia, and hypercapnia that required emergent veno-venous extracorporeal membrane oxygenation support.

Accelerated Marfan syndrome model recapitulates established signaling pathways.

OBJECTIVE: Marfan syndrome (MFS) represents a genetic disorder with a range of clinical features, including proximal aortic aneurysms. Extensive research has revealed an abundance of transforming growth factor beta from a mutation in fibrillin-1 to be the key biochemical mechanism of aneurysm formation. Many important signaling pathways downstream of transforming growth factor beta have been further characterized. Our laboratory has previously demonstrated a unique murine model of MFS resulting in the accelerated formation of ascending aortic aneurysms and dilated cardiomyopathies. This study aims to characterize the relevance of this model to known signaling mechanisms in MFS. METHODS: Fibrillin 1C1039G/+ heterozygous mice (ie, MFS), with a mutation in fibrillin-1, were supplemented with 4.5 mg/kg/d angiotensin II to accelerate aneurysm formation. Four mouse groups were analyzed: wild type with or without angiotensin II and MFS with or without angiotensin II. Aortic tissue from these samples were subjected to western blotting and phosphoimaging to query various signaling pathways. RESULTS: Mice with MFS displayed downstream regulation in both the canonical (Smad2) and noncononical (extracellular signal-regulated kinases and P38) pathways characteristic of MFS. However, these downstream signals were exaggerated in the MFS mice supplemented with angiotensin II (accelerated model), matching the observed phenotypic severity of this model. CONCLUSIONS: The murine MFS model depicted here accelerates ascending aortic aneurysm formation and cardiomyopathies via well-characterized MFS signaling cascades. The mechanistic relevance of the accelerated murine MFS model suggests that it could be an important tool in future studies hoping to characterize MFS signaling in an expedited experimental design.

Insights into Arch Vessel Development in the Bovine Aortic Arch.

A bovine arch is the most common aortic arch variant, characterized by a common origin of the innominate artery and the left common carotid artery. Data have shown that children with bovine arch anatomy and coarctation are at a significantly higher risk of recoarctation following coarctation repair. This study aims to explain the higher coarctation rates, assess the branching of the arch vessels, understand their embryologic origins, and delineate the patterns of displacement of the arch vessels in bovine versus normal anatomy. This retrospective study reviewed the medical records of 178 infants ( < 1-year-old) who had a chest CT Angiogram (58) or CT (120) at our institution between 2007 and 2017. Multiplanar reconstruction software was used to obtain the best image plane to display the sinotubular junction, innominate artery, left common carotid artery, and left subclavian artery. We measured the distances between the branches as HV1, HV2, and HV3. All distances were standardized to body surface area and sinotubular junction diameter, which is a novel method. Bovine arches were found in 32.6% of patients. The total arch length of both arch anatomies was similar. HV3 is longer in bovine arches. HV1 + HV2 and HV2 + HV3 are longer in the normal arches than the bovine arches. The left subclavian artery moves proximally, and the innominate artery moves slightly distally to form the bovine arch and decreasing the clamping distance for coarctation repair. Aortic arch distances were similar when standardized to either sinotubular junction diameter and body surface area.

Bovine arch anatomy influences recoarctation rates in the era of the extended end-to-end anastomosis.

OBJECTIVES: Arch branching has never been shown to influence recoarctation after extended end-to-end anastomosis via thoracotomy, yet in each study bovine arch identification is grossly underreported. This study aims to (1) assess chart review reliability in bovine arch identification; (2) determine recoarctation risk with a bovine arch; and (3) explore an anatomic explanation for recurrent arch obstruction based on arch anatomy. PATIENTS: A total of 49 consecutive patients underwent thoracotomy with extended end-to-end aortic coarctation repair at a single institution (2007-2012). METHODS: Echocardiograms from these patients were reviewed for arch anatomy and compared with the echocardiographic reports. Recurrent arch obstruction was defined as an echocardiographic gradient across the repair of 20 mm Hg or greater. For cases with angiographic images (n = 17), a scaled clamping distance between the left subclavian artery and the maximal proximal clamp location on orthogonal projections was then calculated across arch anatomies. RESULTS: Chart review identified 6.1% (3/49) of patients with a bovine arch compared with 28.6% (14/49) on targeted image review. A total of 28.6% (4/14) of patients with a bovine arch had a follow-up gradient of 20 mm Hg or greater. Only 5.7% (2/35) of patients with normal arch branching had a follow-up gradient of 20 mm Hg or greater. The mean clamping index was significantly diminished in patients with bovine arch anatomy. CONCLUSIONS: Arch anatomy often goes undocumented on preoperative imaging, yet children undergoing extended end-to-end repair with bovine arch anatomy are at a significantly increased risk of recoarctation. This may be due to a reduced clampable distance to facilitate repair. These results should be considered in the preoperative assessment, parental counseling, and surgical approach for children with discrete aortic coarctation.

A Novel Murine Model of Marfan Syndrome Accelerates Aortopathy and Cardiomyopathy.

BACKGROUND: Marfan syndrome (MFS) represents a genetic disorder with variable phenotypic expression. The main cardiovascular sequelae of MFS include aortic aneurysm/dissection and cardiomyopathy. Although significant advances in the understanding of transforming growth factor beta signaling have led to promising therapeutic targets for the treatment of aortopathy, clinical studies have tempered this optimism. In particular, these studies suggest additional signaling pathways that play a significant role in disease progression. To date, studies aimed at elucidating molecular mechanisms involved in MFS-induced disease progression have been hampered by the lack of an accelerated disease model. METHODS: Wild-type B6.129 mice and MFS Fbn1C1039G/+ mice underwent subcutaneous, cervical osmotic minipump installation with sodium chloride (wild-type mice, n = 39; MFS mice, n = 12) or angiotensin II, 4.5 mg/kg daily (wild-type mice, n = 11; MFS mice; n = 35) for as long as 28 days. Hemodynamic measurements were obtained throughout the experiment. Aortas and hearts were analyzed by transthoracic echocardiography and histopathology study. RESULTS: This accelerated murine MFS model replicates increased mortality from MFS-related maladies (20.0%, 39.3%, and 52.9% at 10, 14, and 28 days, respectively). Aortic diameters in accelerated MFS mice were significantly enlarged at 10 days after minipump implantation and correlated with a higher degree of elastin fragmentation. Accelerated MFS mice also demonstrated dilated cardiomyopathy at 14 days, even without aortic insufficiency, suggesting an intrinsic etiology. CONCLUSIONS: A novel in vivo model consisting of subcutaneously delivered angiotensin II in MFS mice reproducibly causes accelerated aortic aneurysm formation and cardiomyopathy. This model allows for better investigation of MFS sequelae by rapid experimental processes.