Post-Esophagogastroduodenoscopy Negative Pressure Pulmonary Edema
Blake Medical Center
critical care, NPPE, negative pressure pulmonary edema, endoscopy - digestive system, duodenoscopy, procedural complications
Internal Medicine | Investigative Techniques | Medicine and Health Sciences | Pulmonology
Negative pressure pulmonary edema (NPPE) is a cause of potentially fatal respiratory failure from exacerbated inspiratory effort against an obstructed airway. Causes of obstruction include anatomical, drug-induced from anesthesia and post-surgical laryngospasm. The incidence of laryngospasm induced pulmonary edema is less known. We present a case of esophagogastroduodenoscopy (EGD) induced laryngospasm with resultant NPPE requiring rapid intubation and management with successful recovery.
A 49-year-old female with history of hypertension, GERD and obstructive sleep apnea presented to an outpatient gastroenterology center for EGD, which was successfully completed. Post procedure, she became hypoxemic on room air, which resolved temporarily with noninvasive positive pressure ventilation; once this was stopped, the patient desaturated. She was transported via EMS to the ED, where she reported voice change and shortness of breath. Pertinent vitals included respiratory rate 30 and oxygen saturation 91% on CPAP. Exam revealed erythematous hard palate and diffusely decreased breath sounds. There was no tongue enlargement or stridor. Nebulized racemic epinephrine and IV solumedrol were given without improvement. She eventually required intubation during which her vocal cords did not appear to be edematous. Chest x-ray showed pulmonary edema. Patient was supported with volume assist control mechanical ventilation. Repeat chest x-ray after lasix revealed resolution of edema. Patient was extubated successfully. Given history and ruled out causes of cardiogenic pulmonary edema, it was determined that the patient had suffered NPPE from laryngospasm after EGD.
Differentials for NPPE include myocardial ischemia, cardiogenic pulmonary edema and anaphylaxis. Patient was euvolemic, had a normal EKG and negative troponins. Echo showed normal ventricular function without valvular abnormalities, ruling out cardiogenic pulmonary edema. Lack of exam findings and peripheral eosinophilia ruled out allergic reaction.
Literature shows an incidence of NPPE of 12% in patients that develop upper airway obstruction; 50% of all cases are known to be from laryngospasm during or post intubation. NPPE is reported to occur after extubation in 74% and during initial airway management in 26% in patients undergoing anesthesia. Due to lack of familiarity, management of NPPE is controversial. Supportive care, noninvasive positive pressure ventilation and possible intubation remain standard of care. Role of furosemide was studied previously, but showed no benefit. Corticosteroids and bronchodilators have not been studied significantly.
Clinicians need to be aware of NPPE for prompt recognition and management of this possibly fatal condition. With more identified cases, there should be further studies on efficacy of medications and their roles in management.
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Publisher or Conference
CHEST Annual Meeting 2019
Khan S, et al. POST-ESOPHAGOGASTRODUODENOSCOPY NEGATIVE PRESSURE PULMONARY EDEMA. Chest. 2019;156(4, Supplement):A2215-A2216. doi:10.1016/j.chest.2019.08.2142