NPPE, also known as postobstructive pulmonary edema, develops in patients with spontaneous respiratory effort who have upper airway obstruction and generate very negative intrathoracic pressure leading to sever hypoxemia and pulmonary edema .
Most children cases of NPPE have been caused by glottis or subglottic obstruction . But causes of adult NPPE are not as same as that of children. The most often reported reason is post-extubation laryngospasm , even the incidence of NPPE is more than 50% among men following laryngospasm . In this case, although there were no apparent causes discussed above, mild collapse of suprasternal fossa and the difficult jaw-thrust during induction phases predicted the possibility of upper airway obstruction. In fact, when unexplained pulmonary edema takes place, NPPE should be considered in the different diagnosis, albeit it is uncommon . In the meanwhile, this case included other similar aspects of NPPE, for example, rapid onset of pulmonary edema after efforts at inspiration against the obstructive airway  and rapid resolves within 12 to 24 hours . In addition, the normal ejection fraction also led us from cardiogenic pulmonary edema to non-cardiogenic pulmonary edema.
In this case, there are other agents to prompt the development of NPPE, such as abnormal hormones and OSA. Because the tumor disturbed the function of pituitary endocrine, so the serum levels of free T4, total T4, cortisol and adrenocorticotropin were abnormal. It has been well known that edema is the most obvious sign of patients with hypothyroidism. If hypothyroidism was severe, cardiogenic pulmonary edema would happen because of the loss of inotropic and chronotropic effects of thyroid hormone . Even non-cardiogenic pulmonary edema could be caused indirectly because hypothyroidism results in the leakage of plasma protein and increases capillary permeability . Meanwhile, hypothyroidism is considered as one potential cause of upper airway obstruction . A variety of factors may be involved, such as alteration in ventilator drive, obesity, and so on . If a patient was with hypothyroidism complication with obesity and OSA, just like this case, there is more probability to develop non-cardiogenic pulmonary edema . In the present case, this girl’s status of OSA was obvious and serious, and her BMI was greater than 35. When the chest CT before operation was reviewed, especially compared to the CT after ICU therapy, it looked as if effusion of both lung fields was more than normal level. If there is unexplained postoperative pulmonary edema in patients without the history of laryngospasm, OSA should be considered as one of culprit [3, 13]. The trait of OSA is frequent episodes of intermittent hypoxia, which leads to pulmonary vascular dysfunction by damaging vascular endothelial cells . On the basis of pulmonary vascular dysfunction, the girl was susceptible to the leaky lung syndrome, which increased the permeability of lung capillaries leading more fluids into the pulmonary interstitium. This might be the reason of increased oxygen and pressure dependency. In fact, these signs predicted severe lung leaking syndrome.
In this case, except hypothyroidism and OSA, serum cortisol and adrenocorticotropin were also significantly lower than the normal level, which are considered as the stress hormone. Its abnormity is a signal of dysfunction of axis of hippocampus-pituitary-adrenal. Patients with hypocortisolism may be more vulnerable to develop lung leaking syndrome. Vice versa, pulmonary edema could be a symptom of adrenal insufficiency. Therefore glucocorticoids have been widely used to treat the syndrome. Clinically, hydrocortisone reduces tracheal aspirate fluid volume and oxygen dependency effectively. And hydrocortisone may improve capillary permeability as well as the inflammation of lung .
In ICU, positive pressure ventilation, diuretics and other treatment were administered. The positive pressure ventilation alleviated negative airway pressure in chest. Diuretics were used for the aim of conservative fluid strategy. Hormone supplementary therapy protected alveolar and vessel endothelial intact. Although the girl recovered as soon as the most cases of NPPE, she had been confronted with severe hypoxemia due to the massive pulmonary edema and shunt. After 5 days of actively supportive care, she was discharged from the ICU.
In current case, although there was no apparent laryngospasm, on the base of mild upper airway obstruction, all other causes, for example hypothyroidism, OSA and hypocortisolism, worked tighter to trigger and accelerate NPPE. So we speculated the pathophysiology of this case was that, the tumor on saddle area damaged pituitary endocrine function to produce body hormones disorder. The abnormity caused body fluid distribution disorder and increased pulmonary capillary permeability. In other words, the tumor made the girl vulnerable to pulmonary edema. At last, the mild upper airway obstruction triggered the cascade of NPPE.
In the present case, there was the biggest regret that the family of the girl rejected second opportunity of operation. But for us, there were some apocalypses. Firstly, we should open mind to look for a pathology that would explain the whole clinical scenario. If second operation had to be taken, the supplement of hormones should be sufficient to sustain electronic at the normal range before the operation. During the process of anesthesia induction, the upper airway should be kept smoothly. The normal ventilation may be the most important to avoid NPPE.