In 2001, 2029 patients underwent surgery at the Victorian Plastic Surgery Unit in Melbourne, Australia. Of these, approximately 50% had cosmetic surgery. In 2 of these cosmetic surgery patients, pulmonary edema associated with laryngospasm developed.

Case 1

A 36-year-old man was admitted for an elective cosmetic rhinoplasty procedure. His medical history included a fractured nose, a shoulder reconstruction, and an appendectomy without complications. He was intubated with a size 8.5 endotracheal tube. Medications included midazolam, propofol, vecuronium, morphine, sevoflurane, droperidol, ondansetron, and clonidine. During surgery, no problems were noted. Oxygen saturation was maintained at more than 97% throughout surgery.

After surgery, in the recovery unit, the patient exhibited a marked cough; his oxygen saturation decreased to 60%, and right-side crepitations were detected on auscultation. Oxygen saturation improved with bag and mask ventilation. Chest radiography revealed bilateral pulmonary congestion. He was reintubated 1 hour after surgery and received 200 mg of furosemide. During reintubation, frothy pink sputum was noted.

Case 2

A 34-year-old woman was admitted for bilateral augmentation mammaplasty and suction-assisted lipoplasty of the thighs and buttocks. She was being treated for depression with sertraline and had mild exercise-induced asthma that was treated with aerolized albuterol. Her history included a rhinoplasty that had resulted in no complications.

Anesthesia, administered with a size 7 endotracheal tube, included midazolam, atracurium, fentanyl, morphine, a N2O/O2 mix, and isoflurane. The intraoperative course was uncomplicated. During extubation she was noted to be coughing while still on the endotracheal tube and biting the tube, causing near-total obstruction. Oxygen saturation at this time was maintained at more than 96%.

Discussion

Background

Negative pressure pulmonary edema (NPPE) is an uncommon condition that occurs in the setting of upper-airway obstruction at the time of emergence from general anesthesia in a spontaneously breathing patient. It is potentially fatal if it goes unrecognized or is misdiagnosed.

Oswalt, in 1977, was the first to report clinical cases of pulmonary edema associated with acute upper-airway obstruction. In 1980, Jackson first described a case of postextubation laryngospasm-induced pulmonary edema. Lang, in 1990, and Deepika, in 1997, reported 77 cases and 30 cases respectively. To our knowledge, no other report of NPPE in a patient undergoing cosmetic surgery has been published.

Although it is a recognized perioperative problem, NPPE is probably underreported and frequently misdiagnosed. The true incidence is not known, but it has been estimated to range from 0.05% to 0.1% of general anesthetic procedures. NPPE has also been referred to by other terms (eg,“laryngospasm-induced pulmonary edema,” “noncardiogenic pulmonary edema,” “obstructive pulmonary edema,” and “postextubation pulmonary edema”), which has contributed to the confusion over its actual incidence. The purpose of this report is to summarize the published data and discuss their implications in the clinical setting of plastic surgery practice.

Pathophysiology

In normal respiration, intrathoracic pressure decreases as the chest wall and diaphragm expand the lungs. In upper-airway obstruction, the patient generates abnormally high negative pressure as he or she attempts to inspire against a closed airway. When this hydrostatic pressure exceeds capillary oncotic pressure, fluid moves out of the vascular space, into the interstitial space, and subsequently the alveoli, resulting in pulmonary edema. The negative pressure also affects the heart by increasing left ventricle afterload and right heart filling, contributing to increasing pulmonary capillary hydrostatic pressure.

Diagnosis

A high degree of suspicion is required for the diagnosis of NPPE. Typically the patient has had an uneventful intraoperative course but stridor, dyspnea, or apnea develops on extubation or soon after. In 80% of patients clinical features are apparent within minutes of airway obstruction or relief of the obstruction. Rarely, onset is delayed by as long as 4 hours. Hypoxemia quickly develops, and the patient’s condition progressively deteriorates despite attempts at ventilation and supplementary oxygen. Crepitations may be audible on auscultation. Frothy pink sputum may be seen if reintubation is needed. Chest radiographs display diffuse pulmonary congestion.

Other causes of hypoxia in the recovery room should be considered. These include aspiration of gastric contents, cardiac failure, volume overload, and pulmonary embolus. The primary differential diagnosis is aspiration pneumonia, even in the absence of observed regurgitation. However, the management of both is initially identical, until evidence of infection is apparent.

Treatment

Most cases of NPPE resolve dramatically within 6 to 24 hours when a patent airway and supplemental oxygen are provided. Lang et al found that 85% of patients required insertion of an endotracheal tube, 50% required ventilation, and 50% required continuous positive airway pressure or positive end-expiratory pressure treatment. McConkey reported that in a series of 6 cases, positive airway pressure was the mainstay of treatment, and only 1 patient required reintubation.

Conclusion

The 2 cases reported here indicate that life-threatening anesthetic complications are possible even in healthy young patients undergoing cosmetic surgery. No obvious pattern of anesthetic techniques or drug administration has been linked with the laryngospasm, except for intubation.