Year : 2014  |  Volume : 17  |  Issue : 3  |  Page : 250--251

Authors' reply: How much evidence is the evidence for a case report?


Prakash K Dubey 
 Department of Anesthesiology and Critical Care Medicine, Indira Gandhi Institute of Medical Sciences, Patna, Bihar, India

Correspondence Address:
Prakash K Dubey
E 3/4, IGIMS Campus, Sheikhpura, Patna - 800 014, Bihar
India




How to cite this article:
Dubey PK. Authors' reply: How much evidence is the evidence for a case report?.Ann Card Anaesth 2014;17:250-251


How to cite this URL:
Dubey PK. Authors' reply: How much evidence is the evidence for a case report?. Ann Card Anaesth [serial online] 2014 [cited 2019 Aug 22 ];17:250-251
Available from: http://www.annals.in/text.asp?2014/17/3/250/135891


Full Text

The Editor,

I thank the editor for giving me an opportunity to respond to the comments. The authors state that negative pressure pulmonary edema (NPPE) is unusual in infants as their chest cage is flexible and the musculature is not fully developed, making their chest walls more compliant. [1] Even with airway obstruction, extreme negative intraalveolar pressure is not generated in the very young pediatric population. [2] After going through Lang's article, [2] I failed to find this evidence in the article. It is interesting to note that in Langs' review of 77 case reports associated with NPPE, 45 patients were pediatric (age <10 years). [2] In fact, in one of the authors references, it was found that in two awake infants (a 4 week and a 6 week old) with total airway obstruction, NPPE developed very rapidly in a matter of seconds during induction of anesthesia. [3] In another of the authors references, a spontaneously breathing 1-month-old infant who was being transferred to the recovery room with a tracheal tube in situ developed NPPE within 30 s secondary to the tracheal tube obstruction. [4] I believe that NPPE in infants has not been widely reported in contemporary literature. Perhaps, the wide spread use of pulse oxymetry and a high degree of awareness and vigilance on the part of pediatric anesthesiologists regarding airway maintenance during induction and recovery from anesthesia may have reduced the incidence of NPPE.

I agree that a chest X-ray obtained immediately during the event would have been supportive. However, presence of froth in the endotracheal tube suction and fine crepitations during chest auscultation were considered sufficient to diagnose and manage the child as a case of NPPE. Moreover, diagnosis of NPPE is usually made on the basis of a history of precipitating incident and symptoms. [5] I agree that data reflecting decreased lung compliance during NPPE would have added to the evidence. The sudden development of the events necessitated urgent maneuvers based on the clinical judgment. At that point of time, we were not aware of the responsible underlying lesion. The proposed mechanism of how this lesion might have caused tracheal obstruction postextubation has been described in the article. The obstruction was relieved in part by tracheal intubation and intermittent positive pressure ventilation; this is evidenced by improvement in SpO 2 from 80% to 92%. Later, a continuous positive airway pressure (CPAP) of 3 cm water was applied cautiously, which resulted in further improvement in SpO 2 . The CPAP would keep the airway open during the expiratory phase also. CPAP is expected to cause a re-expansion of the collapsed alveoli also as suggested by the authors; moreover, CPAP by preventing airway collapse during expiration would allow complete exhalation, decrease in intrinsic positive end-expiratory pressure and improvement in hemodynamics. Here, it is important to note that airway obstruction due to a mediastinal mass varies with the respiratory cycle. [6] During emergence; a diaphragmatic mode of respiration with minimal chest wall motion causes an intrathoracic mass to obstruct the airways which is minimized when the intercostals component become more prominent. [6] The return of a normal tone of bronchial and intercostal muscles over time is expected to increase the lung volume and radial force on airways and play a role in relieving such an airway obstruction.

References

1Kapoor MC: In response to "Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant": Is there reasonable evidence?. Ann Card Anaes 2014;17:249-250
2Lang SA, Duncan PG, Shephard DA, Ha HC. Pulmonary oedema associated with airway obstruction. Can J Anaesth 1990;37:210-8.
3Warner 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.
4Warner LO, Beach TP, Martino JD. Negative pressure pulmonary oedema secondary to airway obstruction in an intubated infant. Can J Anaesth 1988;35:507-10.
5Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth 2011;5:308-13.
6Neuman GG, Weingarten AE, Abramowitz RM, Kushins LG, Abramson AL, Ladner W. The anesthetic management of the patient with an anterior mediastinal mass. Anesthesiology 1984;60:144-7.