Prevalence of Negative-Pressure Pulmonary Edema at an Orthopaedic Hospital

W. Christopher Patton, MD, Champ L. Baker, Jr., MD


J South Orthop Assoc. 2000;9(4) 

In This Article


Negative-pressure pulmonary edema is a potentially dangerous condition with a multifactorial pathogenesis. The central mechanism is a large inspiratory force generated against an obstructed upper airway. The resultant decreased intrathoracic pressure leads to increased venous return to the right side of the heart and increased hydrostatic pulmonary capillary pressure. Further elevating pulmonary capillary pressure is the decreased left ventricular compliance that may result from the right ventricular distention and shift of the cardiac septum to the left. The negative intrathoracic pressure also results in an increased afterload imposed on the left ventricle, causing a further decrease in left ventricular stroke volume.[9,10] Hypoxia induces a massive sympathetic discharge, which produces pulmonary vasoconstriction and increases pulmonary capillary wedge pressure.[11] Thus, the combination of increased venous return and increased pulmonary capillary wedge pressure favors the shift of fluid into the pulmonary interstitium.

All 14 of our cases of NPPE involved postextubation laryngospasm. Other mechanical causes of upper airway obstruction resulting in NPPE include hanging, laryngeal tumor, strangulation, sleep apnea, and biting down on the endotracheal tube while intubated.[1,12,13] Croup and epiglottitis are common causes of upper airway obstruction leading to NPPE in children.[14] Also, Warner et al[15] reported NPPE after administration of muscle relaxants at the beginning of an inhalation induction of anesthesia in healthy infants. The authors postulated that paralysis of glossal muscles occurred before diaphragmatic paralysis, creating an upper airway obstruction.

Negative-pressure pulmonary edema has been subdivided by Guffin et al[16] into two types. Type I occurs immediately after the onset of an acute obstructing event, such as epiglottitis or laryngospasm. Type II occurs after the relief of chronic upper airway obstruction, such as that caused by a laryngeal tumor. Several authors[2,17,18] have suggested that the delay in development of NPPE after the relief of the upper airway obstruction is due to the loss of the "auto-PEEP" phenomenon. Inspiration against the closed glottis is countered by the intermittent expiration against this same closed glottis. This Valsalva's maneuver generates positive pressure to help reduce the transudation of fluid into the interstitium. The relief of the airway obstruction causes a more rapid resolution of the airway pressure than the increased venous hydrostatic pressure.[19]

We found a low prevalence (<0.1%) of NPPE at the Hughston Sports Medicine Hospital. This is, to our knowledge, the first report on the prevalence of NPPE occurring at a hospital specializing in orthopaedic surgery. The prevalence of NPPE in our study was similar to that reported by Deepika et al,[8] who found a prevalence of 0.094% over a 4-year period at their large, metropolitan hospital. All of our cases involved postextubation laryngospasm after an orthopaedic procedure. Most of the cases of NPPE reported by Deepika et al[8] involved laryngospasm, and most occurred in association with head and neck surgery.

Like other authors,[4,5,6] we found that NPPE involved young and healthy patients. However, Deepika et al[8] concluded that NPPE occurred more frequently in healthy men who were middle aged (mean age, 48 years). Yet, no statistical comparison was done between those patients who had NPPE and those who did not. We found that the mean age of those who had NPPE was significantly younger than that of patients having similar procedures who did not have NPPE.

Another similarity to others' findings[4,5,6,7,17] was the good outcome we found with prompt recognition and treatment of NPPE. Of 14 patients, only 3 required brief reintubation. The remainder responded well, and signs and symptoms of NPPE resolved with intravenous diuretic and oxygen therapy. Holmes et al[5] reported that 1 of 8 patients with NPPE required prolonged intubation (3 days). This was the only case in which there was a delay in diagnosis. The physicians postulated that the delay in diagnosis contributed to the prolonged recovery.

Other authors[13,20,21] described less favorable outcomes after NPPE. Goldenberg et al[20] reported one death in six cases of NPPE after otolaryngologic procedures. However, in the remainder of their patients (five of six), NPPE resolved within 24 hours. It was concluded that "a significant complication rate does exist and is generally attributed to a delay in diagnosis."[20] Bonadio and Losek[14] noted that two of five children died after having pulmonary edema and respiratory failure due to upper airway obstruction. Furthermore, Kollef and Pluss[21] found one death in seven cases of NPPE. These cases highlight the need for prompt recognition and treatment of this potentially dangerous condition.

Contrary to other authors,[4,5,6,8] we found that the prevalence of NPPE was not significantly different between male and female patients. Holmes et al[5] reported eight cases of NPPE (seven in adults), all involving male patients. They suggested that athletic male patients were at increased risk because of "their enhanced ability to generate excessive negative intrathoracic pressure."[5] Their eight cases occurred over a 2-year period, between 1987 and 1989. We can only speculate that a longer period of review and a more current review -- reflecting the increased participation of girls and women in athletics -- may account for the differences between our findings and those of Holmes et al.[5] Deepika et al[8] reported that 80% of their cases of NPPE occurred in male patients, but they did not report the total number of male and female patients or compare statistically that number with the number of male versus female patients who had NPPE.

The strengths of our study include the 15-year period of review and the statistical analysis of the differences in age between those who did and those who did not have NPPE. Furthermore, a statistical comparison of the number of male versus female patients who had this potentially dangerous condition was done. This review involves, to our knowledge, the largest number of cases of NPPE involving orthopaedic procedures and is the first review of NPPE at a hospital specializing in orthopaedic surgery.

Weaknesses of our study include the retrospective nature of the study and the possibility of underreporting of cases due to failure to recognize this uncommon condition or errors in coding that would limit recognition during a retrospective review.