NPPO is associated with upper airway obstruction in a spontaneously breathing patient.
It occurs in 0.05–0.1% of all general anaesthetic cases and laryngospasm has been reported as being the cause in 50% of cases.
The clinical course is most frequently observed on emergence from anaesthesia where incomplete recovery from general anaesthesia increases the likelihood of the development of laryngospasm, but it has also been reported after airway obstruction with a foreign body and blockage and biting of tracheal tubes, hanging, and strangulation.
Pulmonary oedema is typically described as developing within 2 min of the obstruction.
Once the airway is occluded, the spontaneously breathing patient will continue to generate negative intrathoracic pressure which will increase substantially as respiratory distress develops.
There is an associated increase in sympathetic tone due to the stress of hypoxia and airway obstruction which increases SVR and elevates pulmonary artery pressure.
This is further exacerbated by hypoxic pulmonary vasoconstriction.
The combination of these processes creates a pressure gradient across the capillary–alveolar membrane which favours the movement of fluid into the lung parenchyma.
It is most common in younger patients, presumably because they are able to generate higher negative inspiratory pressures and, arguably, have a higher sympathetic tone and better cardiac function.
The condition may resolve rapidly after definitive management of the airway obstruction, but in some cases, copious pulmonary oedema may form and it can be associated with pulmonary haemorrhage suggesting capillary membrane damage.
After recognition of the cause of obstruction, the treatment required ranges from relatively modest support such as brief periods of CPAP for 2 h to positive pressure ventilation over a period of 24 h.
Ref: Neurogenic pulmonary edema
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