The Science Journal of the American Association for Respiratory Care

2010 OPEN FORUM Abstracts


Damien P. Beilman1, David L. Acuna3, Roy E. Cole2; 1Respiratory Care, Wesly Medical Center, Wichita, KS; 2Oral and Maxillofacial Associates, Wichita, KS; 3Trauma Services, Wesley Medical Center, Wichita, KS

Introduction: First described in 1836, Ludwig’s Angina is a life threatening cellulitis of the sublingual and submaxillary spaces that can rapidly deteriorate to airway compromise. Negative Pressure Pulmonary Edema (NPPE) was demonstrated in 1927 in spontaneously breathing dogs exposed to high inspiratory resistance. The relationship between negative pressure and the development of pulmonary edema was described in 1942. We present a unique case of non-cardiogenic pulmonary edema with resulting acute lung injury in response to an acute upper airway obstruction that was successfully treated with mechanical ventilation and liberal PEEP. Summary: A 43 year-old male presented to the emergency department in severe respiratory distress with stridor, sternal and intercostals retractions. He had extensive swelling to the face, throat and tongue. Patient was taken emergently to a surgical suite where multiple attempt to both nasally and orally intubate failed. Patient suffered cardiorespiratory arrest and an emergent tracheostomy was performed to which patient responded to in addition to cardiac medications. He then underwent dental extractions and drainage of an abscess of 100 mL of pus. Post-operatively, patient developed hypoxia with P/F ratio of 71 and chest radiograph revealed extensive airspace opacification consistent with pulmonary edema. Patient was diagnosed with acute lung injury secondary to NPPE. Patient was treated with mechanical ventilation and high level PEEP was titrated to maintain adequate oxygenation. Serial chest radiograph showed clearing of infiltrates within 48 hours of insult. Patient was weaned and liberated from mechanical ventilation on post-op day six. Discussion: NPPE has a low prevalence (<0.1%) and is typically seen in post-extubation laryngospasm, but other mechanical obstructions include hanging, laryngeal tumor, biting of endotracheal tube, croup and epiglottis. The primary mechanism postulated is that excessive negative inspiratory pressure leads to increased venous return to the right side of the heart with a concomitant increase in hydrostatic pulmonary capillary pressure. This combination favors the shift of fluid into the alveolar space. Treatment includes relief of the airway obstruction, oxygen therapy and in severe cases, mechanical ventilation and high levels of PEEP. Sponsored Research - None