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University College London, London, UK
Correspondence to: Gareth L. Ackland, PhD, Centre for Anaesthesia, University College London, The Middlesex Hospital, Mortimer St, London W1T 8AA, UK; e-mail: g.ackland{at}rfc.ucl.ac.uk
To the Editor:
Further to the recent review article by Schwarz and Albert1 (April 2004), we would like to add negative pressure pulmonary edema (NPPE) as a further important imitator. NPPE may rarely fall into the category of diffuse alveolar hemorrhage (DAH) through damage of the pulmonary capillaries by mechanical disruption of the alveolar-capillary membrane, resulting in diffuse alveolar injury. More usually, pulmonary edema is manifest, with fulfillment of the clinical, physiologic, and radiographic criteria for acute lung injury (ALI)/ARDS. Several hypotheses have been postulated to explain the pathophysiologic sequelae of NPPE.2345 While early recognition and specific treatment of an underlying condition23456789 may rule in NPPE or rule out other causes of DAH, an obvious underlying cause may be absent particularly after emergence from anesthesia or unwitnessed upper airway obstruction. Indeed, symptoms of NPPE may be considerably delayed after extubation.9 Although symptoms usually resolve rapidly with restoration and/or maintenance of a patent airway and supplemental oxygen, positive end-expiratory pressure and mechanical ventilation may be required for a prolonged period of time.10 Failure to consider NPPE in the differential diagnosis of acute clinical, physiologic, and radiographic changes that fit the criteria for ALI/ARDS may lead to unnecessary and potentially deleterious iatrogenic complications.
References
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