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Negative Pressure Pulmonary Edema after General Anesthesia in a 34-Year-Old Woman

Zachary Mulkey, MD, Texas Tech University Health Sciences Center, Lubbock, TX ; John Batsis, Mayo
Clinic College of Medicine, Rochester, MN ; Michael P. Phy, DO, Texas Tech University Health Sciences
Center, Lubbock, TX ;


Case Presentation: A 34-year-old woman with a history of obesity underwent a right ulnar nerve
exploration and transposition for persistent neuropathic pain and parasthesias. Both axillary block and
general anesthesia were used. Mild stridor was noted at the time of extubation, which was attributed to
laryngospasm. Approximately 40 minutes later she developed bloody secretions and decreasing oxygen
saturations. In the post-anesthesia care unit, her oxygen saturations ranged from 88% to 95% on 10
liters of oxygen per minute by closed face mask and an estimated 20 cc of hemoptysis was observed. An
urgent chest x-ray was obtained which was negative for pneumothorax but did show evidence of
pulmonary edema. The patient was admitted and placed on 10 liters of oxygen by an open face tent
because of her history of claustrophobia. A CT pulmonary angiogram revealed no evidence of pulmonary
embolism. At that time it was thought that the patient had negative pressure pulmonary edema as a
result of taking forceful inspirations following extubation against a closed epiglottis. She improved with
supplemental oxygen, intermittent diuresis and was dismissed on hospital day four.
Discussion : Negative pressure pulmonary edema is an uncommon form of noncardiogenic pulmonary
edema and complication of acute airway obstruction. The incidence of negative pressure pulmonary
edema may be as high as 1 in 1,000 general anesthetic cases and one death so far has been blamed
solely on it. It is more frequently seen in young, healthy patients with no underlying lung disease and is
highly associated with postextubation settings. This patient population may possess the ability to create
the highly negative intrathoracic pressures required to overcome the threshold for pulmonary
microvascular damage. Other contributing factors include obesity, short neck, and obstructive sleep
apnea. Three pathophysiologic mechanisms have been implicated in its etiology: highly negative
intrathoracic pressures, increases in systemic and pulmonary vascular pressures, and a physical
breakdown between the alveoli and capillaries. The resulting edema can be severe and life threatening if
not recognized and treated in a timely fashion. Treatment involves maintaining a patent airway with
adequate oxygenation, fluid restriction and diuretics. Most patients respond quickly and are discharged
within 3 to 4 days.
Conclusion: Hospitalists are increasingly performing perioperative care. This case is intended to raise
hospital physicians’ awareness of negative pressure pulmonary edema and its effects. It is important to
recognize this specific entity and to consider it in the differential diagnosis of acute pulmonary edema in
the perioperative setting.


Author Disclosure Block:


Z. Mulkey, None; J. Batsis, None; M.P. Phy, None.




Society of Hospital Medicine (SHM)
2005 Annual Meeting Abstracts

				
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