Aortic Rupture in a Pediatric Patient With Influenza

Case Report

The association between influenza and cardiac pathology is well-documented.^1–3 Additionally, type A aortic dissections have a higher preponderance during influenza season and it is postulated that influenza may lead to aortic dissection in adults.^4,5 To our knowledge, this association has not been reported in children. Here, we describe a case of aortic rupture in a child with influenza.

A seven-year-old previously healthy female presented to urgent care with a one week history of fever and malaise, and tested positive for influenza A and B. She returned one week later with increased work of breathing and was prescribed dexamethasone and albuterol for presumed reactive airway disease. On her third presentation, she had shortness of breath, presyncope, and persistent chest pain. Chest x-ray revealed (Figure 1) a widened mediastinum. There were diffuse ST elevations on electrocardiogram (EKG) and sinus tachycardia to over 170. A transthoracic echocardiogram showed a large pericardial effusion and a normal aortic arch (Figure 2). She was emergently transferred to our center, received broad-spectrum antibiotics, and underwent pericardiocentesis, yielding 250 mL of straw-colored fluid. Work of breathing and tachycardia improved, but a complex, loculated pericardial effusion remained. In the subsequent 24 hours, she developed worsening tachycardia, bilateral pleural effusions, and an increased oxygen requirement. She was taken to the operating room for a pericardial window through a subxiphoid approach. Notable findings on pericardiotomy included fibrinous material, circumferential clot, and nonpurulent serosanguinous fluid. Hemodynamic improvement was noted during clot and fibrinous material removal, but significant bleeding was encountered with clot removal. The bleeding was temporarily controlled with digital pressure on the ascending aorta. The patient was resuscitated with blood products as a cardiopulmonary bypass machine was brought into the room and was primed. Bilateral femoral cutdowns were performed. The left femoral artery and the right femoral vein were cannulated, and the patient was placed on cardiopulmonary bypass while digital pressure was maintained. Cooling was initiated to deep hypothermia. The subxiphoid incision was then extended superiorly, and a full sternotomy was performed. The aorta was then exposed and a 2.5-cm defect was noted in the anterior ascending aorta roughly 5 mm above the sinotubular junction. The visualized aorta was of normal caliber without gross abnormalities. There was no evidence of dissection, arteritis, purulence, or luminal irregularities. Apart from the obvious defect and a circumferential area of friable aortic tissue that extended roughly 2 mm radially, there were no other obvious abnormalities. Once the aorta was debrided, the defect was repaired using a bovine pericardial patch. The patient was warmed and separated from cardiopulmonary bypass without issue. Notably, serous pleural fluid was determined to be a transudative effusion. Postoperative echocardiogram showed no acceleration of flow across the repair, mild biventricular dysfunction, and resolution of the pericardial effusion. The patient was extubated on postoperative day 1 and had no evidence of neurological injury.

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Figure 1.

Preoperative chest x-ray.

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Figure 2.

Preoperative echocardiogram view of aortic arch.

An extensive workup was performed to investigate etiologies of aortic rupture beyond influenza. Family history did not reveal a predisposition to rheumatologic or cardiac disease. Genetic workup, including whole-exome sequencing, was negative for known variants associated with aortopathy and connective tissue disorders (CTDs). Full-body cross-sectional imaging revealed no evidence of mycotic aneurysms, arteritis, or occult infectious processes. Infectious work-up included negative aerobic, anaerobic, fungal cultures of the pericardium and pleural fluid, and interferon gamma-release assay. Histopathologic examination of the pericardium showed fibropurulent material adherent to the parietal pericardium (Figure 3). The inflammatory infiltrates associated were primarily composed of neutrophils and histocytes and lymphocytes. Fungal and gram stains were negative. There was a persistently thickened pericardium noted on postoperative echocardiogram (Figure 4). While removal of the pericardium to prevent pericardial constriction was considered, further surgical interventions were declined by the family due to the patient's excellent clinical status. The patient was discharged on postoperative day 18 with colchicine for her pericarditis. She was transitioned from intravenous to enteral antibiotics to complete a four-week course of therapy for possible bacterial superinfection as a cause of the rupture. Colchicine was discontinued secondary to gastrointestinal symptoms and improvement in pericardial thickening. At her two-month follow-up appointment, there was complete resolution of pericardial thickening.

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Figure 3.

Histology of the excised pericardium with H&E, x2 magnification.

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Figure 4.

Postoperative echocardiogram demonstrating thick pericardium.

The link between viral infections and aortic dissection is hypothesized to be mediated through a secondary bacterial infection or a nonbacterial inflammatory cascade. Secondary bacterial infection can develop due to a combination of lung epithelial damage and dampening of host immune responses. ⁶ The inflammatory cascade hypothesis proposes increased pro-inflammatory protein expression and indirect vascular inflammation leading to loss of aortic wall integrity. ⁴ Negative tissue cultures in our patient suggest an inflammatory process triggered by initial influenza illness may have been the source of aortic rupture.

Patients with CTD have a known preponderance of aortopathy, as young as five years old. ⁷ Within the aortic pathology spectrum, aortic rupture is the most catastrophic and rare.

Viral complications of influenza have been described, but we could not identify reports of aortic rupture post-influenza in a pediatric patient without a CTD. This case suggests that influenza can lead to life-threatening cardiac sequelae such as aortic rupture, possibly mediated by an inflammatory immune response triggered by influenza infection. The time course of her influenza symptoms supports the hypothesized immune-mediated inflammatory cascade as the source of her pathology. Notably, an immune-mediated pathway has been implicated in multisystem inflammatory syndrome in children associated with preceding SARS-CoV-2 infection. ⁸ In the event of hemodynamically significant pericarditis in a child with influenza, possible vessel wall rupture should be considered, especially in cases of rapid effusion accumulation.