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Table of Contents
LETTER TO EDITOR  
Year : 2014  |  Volume : 17  |  Issue : 3  |  Page : 249-250
In response to "Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant": Is there reasonable evidence?


Department of Anaesthesiology, Saket City Hospital, Saket, New Delhi, India

Click here for correspondence address and email

Date of Web Publication3-Jul-2014
 

How to cite this article:
Kapoor MC. In response to "Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant": Is there reasonable evidence?. Ann Card Anaesth 2014;17:249-50

How to cite this URL:
Kapoor MC. In response to "Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant": Is there reasonable evidence?. Ann Card Anaesth [serial online] 2014 [cited 2019 Dec 11];17:249-50. Available from: http://www.annals.in/text.asp?2014/17/3/249/135890


The Editor,

Negative pressure pulmonary edema (NPPE) results primarily from an airway obstruction during inspiration, when the patient tries to overcome the obstruction with a forced inhalation effort (Muller's maneuver). The resultant high negative intrathoracic pressure (ITP) and a rise in venous return induce hydrostatic transudation of fluid into the extravascular compartment. [1] NPPE develops on relief of the obstruction due to a sudden fall in the ITP. [2] It has been suggested that the etiology of pulmonary edema represents an interplay between several factors, which include cardiogenic and neurogenic mechanisms, as well as hypoxia. [3]

Negative pressure pulmonary edema occurs most often in athletic males. NPPE is unusual in infants as their chest cage is flexible and the musculature is not fully developed, making their chest walls more compliant. Even with airway obstruction, extreme negative intraalveolar pressure is not generated in the very young pediatric population. [4] NPPE in infants has not been widely reported in contemporary literature. NPPE may occur in infants in case the insult of airway obstruction is compounded by application of a negative suction pressure. Suctioning of lavage fluid during bronchoscopy has been reported to cause NPPE by facilitating extravasation of transudate fluid into the alveoli. [5] NPPE in infants has also been reported on restoration of airway after airway obstruction due to falling back of the tongue on induction of anesthesia in infants. [6] A brief (<30 s) period of total airway obstruction in a spontaneously breathing infant can result in fulminant pulmonary edema, with pink frothy secretions appearing in the upper airway. [7]

Dubey reports the occurrence of NPPE in a 3 kg; 3-month-old infant. [8] The author however has not presented evidence of NPPE such as a chest radiograph. An event, lasting such a long duration, should have been documented with a chest X-ray in the least. The author has shown the presence of a posterior mediastinal lesion near the carina and has presumed that it may have caused a bilateral airway obstruction and lead to NPPE. The author has however not highlighted why this lesion caused an airway collapse after tracheal extubation; and why/how this obstruction was relieved and caused NPPE on re-expansion of the lungs thereafter? In case the mediastinal cyst had obstructed the airway, why did the saturation improve on tracheal intubation? The author attributes the relief of the tracheal obstruction to application of a continuous airway positive pressure (CPAP) of 3 cmH 2 O. This does not seem to be a plausible explanation as application of a much higher pressure during intermittent positive pressure ventilation did not relieve it. CPAP may have improved oxygen saturation by aiding the re-expansion of the collapsed alveoli. Return of a normal muscle tone has no role in relieving an intrathoracic obstruction at the level of the carina.

The author should have provided evidence of reduction in lung compliance, after development of NPPE, such as increase in airway pressures, difficulty in achieving adequate tidal volumes/excursions on ventilation or evidence of increased peri-endotracheal tube leak. It is also not understood why the author extubated the trachea, while the infant still had labored breathing, which finally lasted for 6 more h.

 
   References Top

1.Kapoor MC. Negative pressure pulmonary oedema. Indian J Anaesth 2011;55:10-1.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, et al. Clinical and radiologic features of pulmonary edema. Radiographics 1999;19:1507-31.  Back to cited text no. 2
    
3.Holmes JR, Hensinger RN, Wojtys EW. Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991;19:365-71.  Back to cited text no. 3
    
4.Lang SA, Duncan PG, Shephard DA, Ha HC. Pulmonary oedema associated with airway obstruction. Can J Anaesth 1990;37:210-8.  Back to cited text no. 4
    
5.Hannania S, Barak M, Katz Y. Unilateral negative-pressure pulmonary edema in an infant during bronchoscopy. Pediatrics 2004;113:e501-3.  Back to cited text no. 5
    
6.Warner LO, Martino JD, Davidson PJ, Beach TP. Negative pressure pulmonary oedema: A potential hazard of muscle relaxants in awake infants. Can J Anaesth 1990;37:580-3.  Back to cited text no. 6
    
7.Warner LO, Beach TP, Martino JD. Negative pressure pulmonary oedema secondary to airway obstruction in an intubated infant. Can J Anaesth 1988;35:507-10.  Back to cited text no. 7
    
8.Dubey PK. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant. Ann Card Anaesth 2014;17:161-3.  Back to cited text no. 8
[PUBMED]  Medknow Journal  

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Correspondence Address:
Mukul C Kapoor
6, Dayanand Vihar, New Delhi - 110 092
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.135890

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