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.