Discussion
Severe bronchospasm is a rare complication of open-heart surgery (3). However, the outcome can be extremely poor without timely and effective treatment. TAAD is a serious disease, which usually requires emergency surgery with a high rate of perioperative mortality (15). It is a very dangerous condition once the severe bronchospasm occurs following CPB during aortic repair for TAAD. Thus far, no literature has been previously reported on this topic.
Bronchospasm is known to be caused by high airway reactivity. The patient in the current case report presented with a history of asthma for four years, which carried a high probability of airway hyper-responsiveness. Pneumonia could be another inducement of bronchospasm. However, it was impractical to apply adequate dosing and duration of bronchodilator support and antibiotic therapy, because of the cardiac tamponade and unstable hemodynamics in this case.
The diagnosis of bronchospasm should exclude wheezing caused by other diseases, ventilator problems and mechanical obstruction of the airway. Mechanical causes for wheezing include cardiac wheezing and pneumothorax (1). Cardiac wheezing will be accompanied by elevated left atrial pressure and alveolar edema, and pneumothorax is unlikely to involve both lungs. Neither condition was noted in this patient. In addition, the faults of the ventilator and its circuit could lead to ventilator disorders, and the tracheal cannula could be obstructed by mucosal secretions or blood clots, or it could oppressed by the transthoracic echocardiographic probe. We checked the ventilator and its circuit very carefully, following which, no faults were found. In addition, the catheter suction and fiber optic bronchoscopy through the endotracheal tube was performed to rule out tracheobronchial obstruction.
The etiology of severe bronchospasm during CPB remains unclear. Light levels of anesthesia could cause high reactivity of the bronchial smooth muscle cells (16). Moreover, the β-adrenoreceptor antagonist is another trigger of bronchospasm, especially in patients with asthma (2). Deeper anesthetic depth and inhaled β-adrenergic agents are recommended once suspicious bronchospasm occurs. However, neither of these approaches appear to be an appropriate reason that might help explain presentation of bronchospasm in this patient. Drug allergy and transfusions could also induce bronchospasm. However, allergy is usually accompanied by cutaneous allergic manifestations, or cardiovascular abnormality, which did not appear in this patient.
CPB and low core body temperature could be potential triggers in this patient. Activation of the complement component C3a- and C5a-derived anaphylatoxins are known to occur in most patients during CPB, and the pump-oxygenator is the usual site of complement activation (17). Anaphylatoxins are inflammatory mediators that stimulate the release of mast cell-derived histamine, contraction of the bronchial smooth muscle and increases in vascular permeability (18). The levels of C3a and C5a complement components correlate with the duration of CPB (1). Surgery for TAAD is very time-consuming, which could result in systemic inflammatory responses, activation of complement, and activation of thrombin deposition, cytokines, endothelin, endotoxins, and neutrophils (19), which collectively carries a high risk of airway hyper-responsiveness. Decreased temperature might present as an additional inducing stimulus. Joseph Simpson et al., (9) reported on a case of cold-induced bronchospasm during coronary artery bypass surgery. DHCA is commonly used in surgery for TAAD. Although DHCA may preserve better cerebral function during circulatory arrest, the presence of hypothermia could quite possibly trigger bronchospasm in this case, despite there being no direct or firm evidence indicating their relationship. This possibility served to prompt us to consider shortening the duration of CPB and DHCA, which might decrease the incidence of bronchospasm, though it was already very low. Perhaps hemi-arch repair or the branch-first technique (20) could be more beneficial than total arch repair in such cohorts of patients that present with asthma.
Conventional treatments for managing acute bronchospasm include inhaled anesthetics, aerosolized β-adrenergic agents in combination with aminophylline, and intravenous epinephrine and corticosteroid support (1). However, these therapies were of no use to the patient described in this report. The mechanism remains unknown. To address bronchospasm to a more settled pattern, VV-ECMO was performed. ECMO rapidly restores gas oxygenation, corrects respiratory acidosis, removes carbon dioxide, and reverses hemodynamic deterioration, especially for severe refrac¬tory bronchospasm not responding to conventional therapy (21). The patient in the current report, had a good recovery by applying ECMO, showing the excellent effectiveness of this procedure. The inflow site of ECMO should be prudently determined in patients that present with TAAD. Arterial cannulation might potentially aggravate aortic dissection. Therefore, we propose instead of submit that VV ECMO might be a more suitable procedure than veno-arterial ECMO in this patient.