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 the children’s. The most common reported reason for adult experiencing NPPE 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 difficult jaw-thrust during induction phases predicted the possibility of upper airway obstruction. In clinical practice, when unexplained pulmonary edema takes place, NPPE should be considered in different diagnosis, although 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 obstructive airway  and rapid resolves within 12 to 24 h . In addition, normal ejection fraction also led us from cardiogenic pulmonary edema to non-cardiogenic pulmonary edema.
In this case, there were other agents to prompt the development of NPPE, such as abnormal hormones and possible OSA. Because sellar region tumor disturbed function of pituitary endocrine, so the serum levels of free T4, total T4, cortisol and adrenocorticotropin were abnormal. Her serum cortisol and adrenocorticotropin were significantly lower than normal level, which have been well known as stress hormone. And its abnormity is a signal of dysfunction of hippocampus-pituitary-adrenal axis. Patients with hypocortisolism may be more vulnerable to lung leaking syndrome. Vice verse, pulmonary edema may be a symptom of adrenal insufficiency. Therefore glucocorticoids have been widely used to treat this syndrome. Clinically, hydrocortisone effectively reduces tracheal aspirate fluid volume and oxygen dependency. And hydrocortisone may improve capillary permeability as well as lung inflammatory reaction . For this girl, because results of cortisol and adrenocorticotropin were not reported in time, she was not treated with cortisol preoperation. Thus she confronted with the danger developing pulmonary edema before operation. The treatment of cortisol supplement was started in operating-room, following more active cortisol supplement in ICU. Improved serum cortisol level protected alveolar and vessel endothelial intact  to improve pulmonary edema.
Except of cortisol reduction, her free T4 and total T4 were lower than the reference range, which was hypothyroidism. 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 leakage of plasma protein and increases capillary permeability . Additionally, 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, there is more probability to develop non-cardiogenic pulmonary edema . This girl’s weight was 32 kg and BMI was greater than 35, she was not only obese, but also hypothyroidism. And she was with possibility of OSA, so she was coincidence with above situation and vulnerable to non-cardiogenic pulmonary edema.
Before operation, the results of her chest CT on 30th March was negative, which reported by radiology department. However we thought the images of CT showed slight effusion on both lung fields, or more blood in pulmonary circulation. When compared with images of CT on 6th April, the performance of effusion was more obvious on former CT (all of images of chest CT can be obtained from the corresponding author). In fact, this girl’s hormone disorders were able to produce pulmonary edema CT images, there was no contradiction between CT images and her illness. But different photographic condition might cause this deviation of interpretation of chest CT. Whatever results of chest CT, preoperative hormone disorder were putting her to the marginal of pulmonary edema.
In the present case, this girl was obese. And physical examination showed short neck and obvious apnea during sleep. Although there was lack of polysomnograph test, she was great possibility of OSA. If there is unexplained postoperative pulmonary edema in patients without laryngospasm history, OSA should be considered as one of culprits [3, 15]. A trait of OSA is frequent episodes of intermittent hypoxia, which leads to pulmonary vascular dysfunction by damaging vascular endothelial cells . Based on pulmonary vascular dysfunction, this girl was susceptible to leaky lung syndrome. Because destructive vascular endothelial increases permeability of lung capillaries and leads more fluids into pulmonary interstitium. This might be the reason of increased oxygen and pressure dependency. In fact, these signs predicted severe lung leaking syndrome.
The girl was evaluated with Mallamti III preoperatively. And physical examination demonstrated short neck, obese and apnea during sleep. During inhalation induction jaw-thrust was difficult. All these factors indicated the possibility of upper airway obstruction. Mild collapse of suprasternal fossa was another evidence of obstructive upper airway. However there was lack of laryngospasm evidence, because of no signs of larynospasm, such as wheezing rale and stridor. When intubation, no secretion was found on her cords and her glottis opened normally. So larynospasm was not the prior consideration. Although no larynospasm, we suspected mild upper airway obstruction was able to trigger NPPE easily because she possessed too much risks of pulmonary edema.
In ICU, positive pressure ventilation, diuretics and other treatment were administered. 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. Hormones improve pulmonary edema by cAMP-indepentent mechanisms, such as cortisol and thyroid hormone. This girl was not only lack of cortisol, but also free T4 and total T4. So combined administration of them were able to resolve NPPE quickly . Although she recovered as soon as the most cases of NPPE, she had been confronted with severe hypoxemia due to 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 base of mild upper airway obstruction, all other causes, for example hypocortisolism, hypothyroidism, and OSA, worked tighter to trigger and accelerate NPPE. So we speculated the pathophysiology of this case was that, the tumor on sellar region damaged pituitary endocrine function to produce hormones disorder. This abnormity promoted body fluid distribution disorder and increased pulmonary capillary permeability. In other words, the tumor made the girl vulnerable to pulmonary edema. At last, mild upper airway obstruction triggered the cascade of NPPE.
In this case, there was the biggest regret that the girl’s family members 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. Secondly, supplement of hormones should be sufficient to sustain electronic at normal range before operation. Lastly, the process of anesthesia induction, supraglottic airway device should be used to keep airway unobstructed. The normal ventilation may be the most important to avoid NPPE.