We suspect that NPPE after bronchospasm may occur more frequently
Noninvasive positive-pressure ventilation was started with 6 cm H2O of pressure support over 8 cm H2O of positive end expiratory pressure. Consequently, the patient rapidly improved in the PACU, and noninvasive positive pressure ventilation was terminated after 5 h. The following morning the patient was transferred to the gynecology ward and went on to make a full recovery over the next 24 h.
Discussion
We suspect that NPPE after bronchospasm may occur more frequently than reported but goes unrecognized because pulmonary edema after bronchospasm can often be attributed to other factors, such as aspiration, volume overload, or atelectasis. Many patients require oxygen therapy in the PACU, chest radiographs are not routinely obtained, and often NPPE resolves quickly with conservative measures.
The interaction between airway edema and bronchocon-striction raises many issues. The first is whether broncho-constriction could be the root cause of the NPPE. There have been a few theories as to this possibility. Large negative pleural pressures have been measured in children with acute asthma, and this has been shown to be correlated with fluid accumulation in the lungs of dogs. However, asthma is a very heterogeneous disease and bronchoconstric-tion is not uniform in either location or extent. It is possible to close even large central cartilaginous airways with a large enough stimulus, but whether this can happen under clinical conditions is unclear. Although narrowing of large airways occurs in asthma, it is generally believed that it is the additional closure of hundreds or even thousands of small airways leading to air trapping and hyperinflation that causes the clinical signs and symptoms of asthma (Fig 2).
This patient had severe pulmonary disease, a recent decrease in her oral steroid dose, and significant stimulation of her trachea during extubation. This constellation of events could have lead to significant conducting airway narrowing with inadequate airflow during strong inspiratory efforts, leading to the resultant NPPE. A mucus plug could be another inciting factor for the development of her NPPE.